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Decision-making in the management of obesity: a scoping review protocol

Skulsky, Samuel Lamarre 1 ; Kolozsvari, Oana 2 ; Stacey, Dawn 3,4 ; Shorr, Risa 5 ; Gu, Jeffrey 6

1 Department of Surgery, Faculty of Medicine, University of Ottawa, Ottawa, ON, Canada

2 The Ottawa Hospital Bariatric Centre of Excellence, Ottawa, ON, Canada

3 Department of Clinical Epidemiology, University of Ottawa, ON, Canada

4 Ottawa Hospital Research Institute, Ottawa, ON, Canada

5 Learning Services, The Ottawa Hospital, Ottawa, ON, Canada

6 Department of Surgery, University of Saskatchewan, Saskatoon, SK, Canada

Correspondence: Samuel Lamarre Skulsky, [email protected]

The authors declare no conflict of interest.

Objective: 

This scoping review will evaluate the current published literature on decision-making in obesity management.

Introduction: 

Obesity is increasing in incidence worldwide. Although indications have been established for a variety of available treatment modalities, treatment selection must also factor in patient preferences, clinician expertise, and resource availability. Such considerations are crucial given the exponential expansion of new surgical techniques and pharmacologic options in the last decade. Although literature exists for decision-making on various obesity management topics, there are no scoping reviews systematically mapping the literature. This scoping review is timely given that the treatment of obesity has evolved into a multidisciplinary endeavor with myriad management decisions that both patients and clinicians must navigate.

Inclusion criteria: 

The review will consider for inclusion full-text primary studies, published in English from the year 2000 onwards, pertaining to decision-making in obesity management for health care providers involved in obesity management for patients aged ≥18 years.

Methods: 

This scoping review will be conducted in accordance with the JBI methodology for scoping reviews. Embase (Elsevier), MEDLINE (PubMed), Scopus (Elsevier), Web of Science (Clarivate), CINAHL Complete (EBSCO), PsycINFO (EBSCO), and Cochrane Central (Wiley) will be systematically searched using a predefined strategy. Two independent reviewers will conduct a 3-tiered screen of identified articles, with a third reviewer resolving disputes. Data extraction will be performed using a predefined, yet flexible form. Descriptive summaries and mapping will be provided for included studies. Available evidence and knowledge gaps will be identified and summarized as they relate to specific concepts, populations, and contexts in obesity management decision-making.

Introduction

Obesity, defined as a body mass index (BMI) greater or equal to 30 kg/m 2 , is a chronic disease increasing in prevalence worldwide. 1 There are multiple treatment modalities for managing obesity, including surgery, pharmacological treatments, medical management, as well as behavioral modifications. Each treatment modality varies in efficacy, complications, side effects, long-term follow-up requirements, and cost, all of which may affect treatment choice. 2 These modalities can be used individually or in combination. Patients and clinicians must navigate the increasing array of management options to select an appropriate treatment plan that aligns with the patients’ values and overall goals. Improved decision-making processes may lead to improved treatment decisions and patient satisfaction.

Pharmacological agents can affect weight loss and ameliorate obesity-related comorbidities, often as adjuncts to other treatment modalities. Liraglutide and semaglutide are glucagon-like peptide-one (GLP-1) receptor agonists that demonstrate efficacy in producing clinically significant weight loss in patients with or without concomitant diabetes. 3 The combination drug naltrexone/bupropion also offers good initial weight loss. 4 In contrast to surgery, data on long-term weight loss for these medications are lacking. However, 1-year outcomes demonstrate 18%, 24%, and 15% excess weight loss for liraglutide, semaglutide, and naltrexone/bupropion, respectively. 3,5,6 However, pharmacological options may be limited by side effects and require long-term adherence, thus carrying an associated lifelong financial cost. Discontinuation of pharmacological therapy leads to weight regain and reversal of comorbidity resolution. 7

Medical management is another approach for obesity management. Although inconsistent, the literature generally equates “medical management” to medically supervised diets. Medical management can provide rapid weight loss for preoperative optimization (both bariatric and non-bariatric procedures) and is less invasive than bariatric surgery or pharmacotherapy. 8,9 Medical management focuses on caloric restriction, whether through balanced low-calorie diets, carbohydrate or fat restriction, increased protein intake combined with reduced calories, or intermittent fasting. 9 The most consistently successful diet is the very low-calorie diet (VLCD), constraining patients to 200 to 800 daily calories. In 1 review article, initial weight loss (%IWL) for the VLCD at 6 and 12 months was 16% and 10%, respectively. 10 However, VLCDs may not confer superior long-term weight loss compared with conventional diets. In a 2012 meta-analysis of VLCDs, mean %IWLs of 6% and 5% were reported for VLCDs and LCDs, respectively (mean follow-up 1.9 +/− 1.6 years). 11 Side effects from dietary approaches include hair loss, sensation of being cold, and thinning of the skin, among other symptoms. 9

Behavioral modification (also known as behavioral therapy) is another approach, used either as a primary treatment option or incorporated into a multi-modal treatment program. Behavioral modification aims for sustained weight loss by helping patients modify patterns of food intake and physical activity as well as helping address cues and/or environmental stimuli that may prompt overeating. 8 Behavior modification has been shown to improve weight loss achieved with other treatment modalities, such as dietary and pharmacological therapy. 12 Behavioral modification is provided in multiple contexts: patients may utilize established treatment programs involving direct interaction with registered dietitians, psychiatrists, and psychologists, although self-help or commercial weight-loss programs exist as do technology-based approaches such as mobile applications. 13 Regardless of the specific modality, patient adherence is a key determinant of successful weight loss when applying behavior modification. In the Look AHEAD study, obese adults with type 2 diabetes mellitus assigned to intensive behavioral modification demonstrated greater clinically significant weight loss 8 years later compared with patients assigned to upfront support groups and basic education. 14

Bariatric surgery is the most effective treatment for obesity and facilitates remission of obesity-associated comorbidities. 15 It is typically reserved for patients with a BMI ≥ 40 or for patients with a BMI ≥ 35 with obesity-related comorbidities. The 2 most common operations are the vertical sleeve gastrectomy (VSG) and the Roux-en-Y gastric bypass (RYGB). 16 However, other bariatric procedures are gaining popularity, such as the duodenal switch. 16,17 Of the obesity management options, surgery offers the best long-term sustained weight loss and comorbidity resolution. Percent excess weight loss at 10 years is approximately 60%, 56%, and 74% for the VSG, RYGB, and duodenal switch, respectively. 18 Ten-year diabetes remission rates for RYGB and duodenal switch were 25% and 50%, respectively. 15 Although contemporary 30-day post-operative mortality rates and post-operative morbidity rates are 0.2% and 3%, respectively, 19 patients still assume this risk. Furthermore, each surgery carries its own complication profile and requires permanent adjustments, such as dietary changes and lifelong vitamin supplementation.

Decision-making in the management of obesity should ideally account for multiple factors, starting with which treatment modalities to pursue, while incorporating patient preferences and values along with those of their health care providers. Additional factors to consider include patient medical/surgical history, willingness to implement dietary and behavioral changes, expected outcomes, treatment risk profiles/side effects, ability to participate in pre- and post-operative care, fitness for surgery, as well as clinician expertise, financial considerations, and health care system resource constraints.

An important concept in decision-making is shared decision-making (SDM), a collaborative process in which both the health care provider and the patient participate in deciding on a particular treatment. The health care worker, guided by empirical evidence, provides an overview of available treatments and their alternatives, expected outcomes, and risks. Ideally, this facilitates the selection of a treatment aligned with the patient's core values, preferences, and personal or cultural beliefs. 20 Nevertheless, research suggests that SDM is inconsistently applied in health care 21 ; however, within the field obesity management, researchers and clinicians are highlighting the applicability of SDM. Already, SDM has been studied for various decisions required in obesity management, including the decision to initiate treatment, 22 initiate healthy behavioral changes, 23 choose a specific surgical procedure, 24 and select appropriate pharmacotherapy. 25

Clinicians also grapple with patient misconceptions and health care providers who may act as “barriers” to pursuing appropriate treatment. For example, 1 study of family physicians revealed that 52% were not aware that the contemporary mortality rate is less than 1% for bariatric surgery. This is striking given that, in the same study, the most common reason for non-referral was “potential for complications and death.” 26 Similarly, patient misconceptions surrounding obesity management are common. With bariatric surgery, for example, a lack of familiarity with post-operative morbidity and mortality rates, surgical candidacy, realistic weight loss expectations, and post-operative lifestyle changes are frequently encountered. 27 As a result, a patient's desired treatment and outcomes might not align. For example, 1 study reported on a subgroup of patients desiring a laparoscopic adjustable gastric band despite having “maximum weight loss” as their stated top priority; laparoscopic adjustable gastric bands do not provide the greatest degree weight loss. 24 This exemplifies the need for patient education in addition to determination of a patient's preferential values when selecting an appropriate treatment.

Patient decision aids are interventions that facilitate SDM, providing information on options, benefits and harms, and helping patients clarify their values for outcomes. 28 In addition to helping patients assume an active role in decision-making, decision aids improve their knowledge and set realistic expectations, lower decisional conflict, and enhance agreement between the option chosen and patients’ values. 29 Within the field of obesity management, the study of decision aids has focused on surgical decision-making, 29 although some research addresses multiple treatment modalities. 30,31

Given the expanding list of management options for obesity that both clinicians and patients must navigate, treatment decisions are becoming increasingly complex. Thus, our scoping review is timely and aims to determine the current body of knowledge on decision-making in obesity management. Specifically, we seek to clarify the types of decisions that have been studied, including referral versus treatment decisions from primary care providers, decisions on which categories of treatment to pursue (eg, pharmacotherapy vs surgical management or both), and deciding on treatment options within a category (eg, which surgery to choose). In clarifying the types of decisions explored in the literature, we also wish to determine the health care contexts in which these decisions have been studied, ranging from primary to specialist care. We also wish to identify studies on decision aids and SDM in obesity management, and determine which of the abovementioned types of decisions were examined.

As described, both patients and health care providers may misunderstand the risks and benefits associated with specific obesity treatment modalities. 24,26,27 Furthermore, other factors may hinder patients from pursuing specific treatments, including financial burden or the inability to quit smoking (smoking cessation is a common requirement for undergoing bariatric surgery). 32 This scoping review seeks to identify the existing primary studies on these barriers to optimal obesity management.

In addressing these questions, this scoping review ultimately aims to identify knowledge gaps in decision-making research for obesity management, with the goal of directing future research to decisions that have been understudied. Additionally, in identifying the barriers to obesity management reported in the literature, we hope to highlight factors that either require further study or could be considered by future researchers for incorporation into new decision-making tools. A search of Google Scholar, MEDLINE (PubMed), and JBI Evidence Synthesis did not identify any published or in-progress scoping reviews that address this topic in the manner proposed by our current protocol. The value of undertaking this scoping review is that it can help direct future research on decision-making in obesity and facilitate future care for patients suffering from a disease that is reaching epidemic proportions.

Review questions

What is the status of current knowledge in the published literature about decision-making in the management of obesity in relation to those involved in treatment decisions (eg, patients, clinicians) and the various clinical settings in which management decisions are made?

Sub-questions include:

• i) In the setting of obesity management, how is decision-making defined in the literature and what types of decisions have been examined?
• ii) What published literature exists on obesity management decision aids and what treatment modalities are addressed in these aids?
• iii) What published literature exists on SDM for patients and clinicians in obesity management and who are the individuals under study?
• iv) What barriers to decision-making are reported by the obesity management literature?

Inclusion criteria

The inclusion criteria have been developed using the PCC framework 33 and are outlined below.

Participants

This review will include studies examining individuals involved in obesity management, either as clinicians or as recipients of treatment. Relevant individuals include adult patients (≥ 18 years of age) living with obesity (BMI ≥ 30), primary care providers, bariatric medicine clinicians, bariatric surgeons, and multidisciplinary allied health staff, including, but not limited to, psychiatrists, psychologists, nurses, and dietitians. The reason for excluding patients ≥ 18 years is that, despite increasing acceptance, controversy still exists surrounding bariatric surgery for minors, with many pediatric practitioners reporting that they would not refer their patients for surgical consultation. 34 Furthermore, pediatric patients face relatively greater challenges with access to bariatric surgical programs compared with their adult counterparts. 34 Although it is just 1 option for managing obesity, the difference in attitudes and access to bariatric surgery between minors and adults is such that a scoping review on decision-making in obesity management for pediatric patients should be a separate undertaking.

This review will examine studies on decision-making in obesity management. In general, decision-making is a cognitive process of choosing 1 course of action from several possibilities. 35 This will be our working definition when considering whether a potential source is addressing decision-making. When making a decision, the best available evidence is applied within the constraints of available clinical expertise and resources, while accounting for patient and provider preferences. In medical literature, a precise taxonomy for the various kinds of decisions made in health care is not consistently applied, 36 therefore, a study's use of the term “decision-making” can refer to myriad different types of decisions (eg, treatment decisions, choosing an investigation, choosing to consult a specialist). As such, this scoping review also aims to clarify what exactly is being studied in the decision-making literature within the field of obesity management.

A sub-categorization of decision-making important to this review is the concept of SDM. In contrast to “decision-making,” SDM is a more concrete term that has been defined as a collaborative process in which both the clinician and patient participate in arriving at a particular treatment. The clinician, informed by empirical evidence, provides an overview of available treatments and the associated risks and benefits while the patient shares their core values, preferences, and personal or cultural beliefs in order to arrive at a mutually shared treatment decision. 20 Similarly to SDM, “decision aids” is a well-defined term, and is considered interventions that facilitate SDM by making explicit the decision, providing information on options, benefits, and harms, and helping patients clarify their values for outcomes. 28

The concept of treatment modalities for obesity also requires definition to ensure clarity and a common language for the scoping review. For example, “medical management of obesity” is inconsistently defined; in the literature it has been used interchangeably to refer to medically supervised diets or pharmacological treatments. For the purposes of this review, we will categorize treatment modalities as falling into one of the following categories: surgical management, pharmacological treatments, medical management (meaning medically supervised diets), and behavioral interventions (inclusive of psychiatric and psychological management, and exercise therapy).

For the purposes of this review, a “barrier” to decision-making will be defined as any factor that might affect pursual of evidence-based management of obesity. For example, a barrier could be a primary care physician's misunderstanding of complication rates for bariatric surgery or patient unfamiliarity with treatment options.

This review aims to capture decision-making in obesity management in all health care settings where care may be provided, on a continuum from primary to quaternary care. For example, in a primary care context, possible decisions may be whether to initiate lifestyle interventions or to refer the patient to a specialized treatment center. At the tertiary level, the decisions may be focused on choosing a combination of surgical, pharmacological, medical, and behavioral interventions. This scoping review will not focus on decision-making research in the context of experimental treatments and will thus be restricted to research focusing on currently accepted treatments. Observational decision-making research, as well as controlled experiments on decision-making for currently accepted treatments, will be considered. From a geographic/cultural perspective, we will not consider decision-making research examining traditional, natural, or cultural treatment modalities without peer-reviewed evidence of their efficacy. Two of the authors (JG, NK) of this scoping review protocol are experts in obesity management; if they are unable to ascertain whether a particular treatment is sufficiently evidence-based, we will consult our multidisciplinary colleagues to determine whether the treatment is backed by evidence or is commonly used.

Types of sources

This scoping review will consider primary research studies with quantitative, qualitative, and mixed methods study designs. Opinion articles, letters to the editor, book chapters, systematic reviews, narrative reviews, clinical reviews, and consensus guidelines will not be included. However, all sources that are captured by our search will have their references examined for potential primary studies to include.

The proposed scoping review will be conducted in accordance with the JBI methodology for scoping reviews. 33

Search strategy

The search strategy will aim to locate published primary studies. In collaboration with a research librarian familiar with academic and clinical health care research, an initial limited search of Embase (Elsevier), MEDLINE (PubMed), Scopus (Elsevier), Web of Science (Clarivate), CINAHL Complete (EBSCO), PsycINFO (EBSCO), and Cochrane Central (Wiley) was undertaken using preliminary keywords relating to our population, context, and concepts described above. A list of the text words contained in the titles and abstracts of relevant articles, as well as the index terms used to describe those words, was compiled. Synonyms and interchangeable terms for these keywords were also collected. Using these terms, we performed a search of CINAHL Complete (EBSCO; see Appendix I). Gray literature and/or media will not be included; this scoping review is focused on peer-reviewed literature that is readily accessible to those with interest in decision-making research. The reference lists of articles selected for full-text review will be screened for additional papers. The study reviewers intend to contact authors of primary studies if information relevant to our planned data extraction is missing.

We will restrict our final analysis to articles published in English as a matter of convenience and to avoid interpretative errors in attempted translation. We recognize the potential for language bias; therefore, the initial search will include articles written in any language to quantify the extent of non-English literature excluded from our analysis.

Study selection

All identified records will be collated and uploaded into DistillerSR (Evidence Partners, Ottawa, Canada) and duplicates will be removed. Two primary reviewers (SS, JG) will independently screen all articles in 3 stages: title screening, abstract screening, and full-text screening. Standardized forms created in DistillerSR will facilitate the screening process. As part of an inclusive strategy, agreement from both primary reviewers will be required for an article to be excluded at the title-screening stage. During the abstract and full-text screening stages, conflicts will be flagged for a third expert reviewer (NK) to resolve. Articles will only be included in our analysis if they meet the following criteria: they relate to the management of obesity, are associated with a full-text article of a primary study (no abstract-only search results, guidelines, opinions, or book chapters), are written in English, published in 2000 or later, and pertain to individuals 18 years or older.

Searches will be limited to the year 2000 or later as many pharmacotherapeutic and surgical treatments for obesity prior to the 2000s are either no longer in use or have drastically limited indications, and this review aims to examine decision-making research in the context of the modern era of obesity management. Furthermore, the modern morbidity and mortality rates for today's surgical procedures are sufficiently low that the decision to proceed with surgery now is a different discussion to what it has been in the past. 37

Articles selected following full-text screening will be retrieved and their citation details imported into the JBI System for the Unified Management, Assessment and Review of Information (JBI SUMARI; JBI, Adelaide, Australia). 38 See Appendix II for the screening questions. Reasons for exclusion of full-text papers will be recorded and reported in the final review. The results of the search will be presented in a Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) flow diagram. 39

Data extraction

Data will be extracted by 2 independent reviewers (JG, SS) using the questions in Appendix III. Details about the population, the treatment modalities, and context relevant to the review questions will be extracted. Additional data points will include author details, year and type of publication, country of origin, study aims, methodology, and key findings. For publications investigating a decision aid, the type of aid (eg, video, pamphlet, interactive chart) as well as its components will be recorded. Revision of the data extraction tool during the extraction process will be iterative, but prior to beginning the data extraction process, we will conduct a calibration exercise (pilot test), as outlined by Tricco et al. 40 Any disagreements that arise between the reviewers will be resolved through discussion or with a third reviewer. Authors of papers will be contacted to request missing or additional data, whenever necessary.

Data analysis and presentation

The analysis for this scoping review will predominantly consist of a summative approach for the data extracted from the published literature.

If provided, definitions of decision-making in obesity management settings will be extracted verbatim from identified sources and summarized in tabular format. References cited to support these definitions will also be presented. The actual decisions being examined by each study will be summarized as well.

Regarding decision aids, a tabular format will be used to highlight the types of aids studied and the treatment modalities they address. Regarding SDM, tabular format will be used to summarize the existing research and the individuals involved in the SDM process (eg, patients, clinicians).

Barriers that have been reported as having an impact on decision-making in obesity management research will be summarized with the frequency of selected studies that examine each barrier. If necessary, descriptive qualitative content analysis may be used to code barriers into overall categories to facilitate a useful presentation of the results. The anticipated broad categories may include concerns over financial considerations, outcomes, treatment risks, changes in lifestyle, and necessary time commitment.

To supplement our in-text discussion, overview graphs or diagrams will be used as appropriate to highlight research gaps pertaining to our review questions, in particular gaps in decision-making research regarding specific treatment modalities, health care contexts, and populations.

Author contributions

JG, SS, NK, DS contributed to the writing of the manuscript. SS, JG, NK, DS, RS contributed to the design of the protocol. RS, SS devised the search strategy and conducted the preliminary search. JG, SS, RS created the data extraction tool.

Appendix I: Search strategy

Cinahl complete (ebsco).

Date searched: January 12, 2022

Appendix II: Article screening strategy and questions

Appendix III: Draft data extraction instrument

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How To Write A Strong Obesity Research Paper?

Table of Contents

Obesity is such a disease when the percent of body fat has negative effects on a person’s health. The topic is very serious as obesity poisons the lives of many teens, adults and even children around the whole world.

Can you imagine that according to WHO (World Health Organization) there were 650 million obese adults and 13% of all 18-year-olds were also obese in 2016? And scientists claim that the number of them is continually growing.

There are many reasons behind the problem, but no matter what they are, lots of people suffer from the wide spectrum of consequences of obesity.

Basic guidelines on obesity research paper

Writing any research paper requires sticking to an open-and-shut structure. It has three basic parts: Introduction, Main Body, and Conclusion.

According to the general rules, you start with the introduction where you provide your reader with some background information and give brief definitions of terms used in the text. Next goes the thesis of your paper.

The thesis is the main idea of all the research you’ve done written in a precise and simple manner, usually in one sentence.

The main body is where you present the statements and ideas which disclose the topic of your research.

In conclusion, you sum up all the text and make a derivation.

How to write an obesity thesis statement?

As I’ve already noted, the thesis is the main idea of your work. What is your position? What do you think about the issue? What is that you want to prove in your essay?

Answer one of those questions briefly and precisely.

Here are some examples of how to write a thesis statement for an obesity research paper:

• The main cause of obesity is determined to be surfeit and unhealthy diet.
• Obesity can be prevented no matter what genetic penchants are.
• Except for being a problem itself, obesity may result in diabetes, cancers, cardiovascular diseases, and many others.
• Obesity is a result of fast-growing civilization development.
• Not only do obese people have health issues but also they have troubles when it comes to socialization.

20 top-notch obesity research paper topics

Since the problem of obesity is very multifaceted and has a lot of aspects to discover, you have to define a topic you want to cover in your essay.

How about writing a fast food and obesity research paper or composing a topic in a sphere of fast food? Those issues gain more and more popularity nowadays.

A couple of other decent ideas at your service.

• The consequences of obesity.
• Obesity as a mental problem.
• Obesity and social standards: the problem of proper self-fulfilment.
• Overweight vs obesity: the use of BMI (Body Mass Index).
• The problem of obesity in your country.
• Methods of prevention the obesity.
• Is lack of self-control a principal factor of becoming obese?
• The least obvious reasons for obesity.
• Obesity: the history of the disease.
• The effect of mass media in augmentation of the obesity level.
• The connection between depression and obesity.
• The societal stigma of obese people.
• The role of legislation in reducing the level of obesity.
• Obesity and cultural aspect.
• Who has the biggest part of the responsibility for obesity: persons themselves, local authorities, government, mass media or somebody else?
• Why are obesity rates constantly growing?
• Who is more prone to obesity, men or women? Why?
• Correlation between obesity and life expectancy.
• The problem of discrimination of the obese people at the workplace.
• Could it be claimed that such movements as body-positive and feminism encourage obesity to a certain extent?

Best sample of obesity research paper outline

An outline is a table of contents which is made at the very beginning of your writing. It helps structurize your thoughts and create a plan for the whole piece in advance.

…Need a sample?

Here is one! It fits the paper on obesity in the U.S.

Introduction

• Hook sentence.
• Thesis statement.
• Transition to Main Body.
• America’s modern plague: obesity.
• Statistics and obesity rates in America.
• Main reasons of obesity in America.
• Social, cultural and other aspects involved in the problem of obesity.
• Methods of preventing and treating obesity in America.
• Transition to Conclusion.
• Unexpected twist or a final argument.
• Food for thought.

Specifics of childhood obesity research paper

A separate question in the problem of obesity is overweight children.

It is singled out since there are quite a lot of differences in clinical pictures, reasons and ways of treatment of an obese adult and an obese child.

Writing a child obesity research paper requires a more attentive approach to the analysis of its causes and examination of family issues. There’s a need to consider issues like eating habits, daily routine, predispositions and other.

Top 20 childhood obesity research paper topics

We’ve gathered the best ideas for your paper on childhood obesity. Take one of those to complete your best research!

• What are the main causes of childhood obesity in your country?
• Does obesity in childhood increase the chance of obesity in adulthood?
• Examine whether a child’s obesity affects academic performance.
• Are parents always guilty if their child is obese?
• What methods of preventing childhood obesity are used in your school?
• What measures the government can take to prevent children’s obesity?
• Examine how childhood obesity can result in premature development of chronic diseases.
• Are obese or overweight parents more prone to have an obese child?
• Why childhood obesity rates are constantly growing around the whole world?
• How to encourage children to lead a healthy style of life?
• Are there more junk and fast food options for children nowadays? How is that related to childhood obesity rates?
• What is medical treatment for obese children?
• Should fast food chains have age limits for their visitors?
• How should parents bring up their child in order to prevent obesity?
• The problem of socializing in obese children.
• Examine the importance of a proper healthy menu in schools’ cafeterias.
• Should the compulsory treatment of obese children be started up?
• Excess of care as the reason for childhood obesity.
• How can parents understand that their child is obese?
• How can the level of wealth impact the chance of a child’s obesity?

Childhood obesity outline example

As the question of childhood obesity is a specific one, it would differ from the outline on obesity we presented previously.

Here is a sample you might need. The topic covers general research on child obesity.

• The problem of childhood obesity.
• World’s childhood obesity rates.
• How to diagnose the disease.
• Predisposition and other causes of child obesity.
• Methods of treatment for obese children.
• Preventive measures to avoid a child’s obesity.

On balance…

The topic of obesity is a long-standing one. It has numerous aspects to discuss, sides to examine, and data to analyze.

Any topic you choose might result in brilliant work.

How can you achieve that?

Follow the basic requirements, plan the content beforehand, and be genuinely interested in the topic.

Option 2. Choose free time over struggle on the paper. We’ve got dozens of professional writers ready to help you out. Order your best paper within several seconds and enjoy your free time. We’ll cover you up!

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Obesity Essay

Last updated on: Feb 9, 2023

Obesity Essay: A Complete Guide and Topics

By: Nova A.

11 min read

Reviewed By: Jacklyn H.

Published on: Aug 31, 2021

Are you assigned to write an essay about obesity? The first step is to define obesity.

The obesity epidemic is a major issue facing our country right now. It's complicated- it could be genetic or due to your environment, but either way, there are ways that you can fix it!

Learn all about what causes weight gain and get tips on how you can get healthy again.

On this Page

What is Obesity

What is obesity? Obesity and BMI (body mass index) are both tools of measurement that are used by doctors to assess body fat according to the height, age, and gender of a person. If the BMI is between 25 to 29.9, that means the person has excess weight and body fat.

If the BMI exceeds 30, that means the person is obese. Obesity is a condition that increases the risk of developing cardiovascular diseases, high blood pressure, and other medical conditions like metabolic syndrome, arthritis, and even some types of cancer.

Obesity Definition

Obesity is defined by the World Health Organization as an accumulation of abnormal and excess body fat that comes with several risk factors. It is measured by the body mass index BMI, body weight (in kilograms) divided by the square of a person’s height (in meters).

Obesity in America

Obesity is on the verge of becoming an epidemic as 1 in every 3 Americans can be categorized as overweight and obese. Currently, America is an obese country, and it continues to get worse.

Paper Due? Why Suffer? That's our Job!

Causes of obesity

Do you see any obese or overweight people around you?

You likely do.

This is because fast-food chains are becoming more and more common, people are less active, and fruits and vegetables are more expensive than processed foods, thus making them less available to the majority of society. These are the primary causes of obesity.

Obesity is a disease that affects all age groups, including children and elderly people.

Now that you are familiar with the topic of obesity, writing an essay won’t be that difficult for you.

How to Write an Obesity Essay

The format of an obesity essay is similar to writing any other essay. If you need help regarding how to write an obesity essay, it is the same as writing any other essay.

Obesity Essay Introduction

The trick is to start your essay with an interesting and catchy sentence. This will help attract the reader's attention and motivate them to read further. You don’t want to lose the reader’s interest in the beginning and leave a bad impression, especially if the reader is your teacher.

A hook sentence is usually used to open the introductory paragraph of an essay in order to make it interesting. When writing an essay on obesity, the hook sentence can be in the form of an interesting fact or statistic.

Head on to this detailed article on hook examples to get a better idea.

Once you have hooked the reader, the next step is to provide them with relevant background information about the topic. Don’t give away too much at this stage or bombard them with excess information that the reader ends up getting bored with. Only share information that is necessary for the reader to understand your topic.

Next, write a strong thesis statement at the end of your essay, be sure that your thesis identifies the purpose of your essay in a clear and concise manner. Also, keep in mind that the thesis statement should be easy to justify as the body of your essay will revolve around it.

Body Paragraphs

The details related to your topic are to be included in the body paragraphs of your essay. You can use statistics, facts, and figures related to obesity to reinforce your thesis throughout your essay.

If you are writing a cause-and-effect obesity essay, you can mention different causes of obesity and how it can affect a person’s overall health. The number of body paragraphs can increase depending on the parameters of the assignment as set forth by your instructor.

Start each body paragraph with a topic sentence that is the crux of its content. It is necessary to write an engaging topic sentence as it helps grab the reader’s interest. Check out this detailed blog on writing a topic sentence to further understand it.

End your essay with a conclusion by restating your research and tying it to your thesis statement. You can also propose possible solutions to control obesity in your conclusion. Make sure that your conclusion is short yet powerful.

Obesity Essay Examples

Essay about Obesity (PDF)

Childhood Obesity Essay (PDF)

Obesity in America Essay (PDF)

Essay about Obesity Cause and Effects (PDF)

Satire Essay on Obesity (PDF) 

Obesity Argumentative Essay (PDF)

Obesity Essay Topics

Choosing a topic might seem an overwhelming task as you may have many ideas for your assignment. Brainstorm different ideas and narrow them down to one, quality topic.

If you need some examples to help you with your essay topic related to obesity, dive into this article and choose from the list of obesity essay topics.

Childhood Obesity

As mentioned earlier, obesity can affect any age group, including children. Obesity can cause several future health problems as children age.

Here are a few topics you can choose from and discuss for your childhood obesity essay:

• What are the causes of increasing obesity in children?
• Obese parents may be at risk for having children with obesity.
• What is the ratio of obesity between adults and children?
• What are the possible treatments for obese children?
• Are there any social programs that can help children with combating obesity?
• Has technology boosted the rate of obesity in children?
• Are children spending more time on gadgets instead of playing outside?
• Schools should encourage regular exercises and sports for children.
• How can sports and other physical activities protect children from becoming obese?
• Can childhood abuse be a cause of obesity among children?
• What is the relationship between neglect in childhood and obesity in adulthood?
• Does obesity have any effect on the psychological condition and well-being of a child?
• Are electronic medical records effective in diagnosing obesity among children?
• Obesity can affect the academic performance of your child.
• Do you believe that children who are raised by a single parent can be vulnerable to obesity?
• You can promote interesting exercises to encourage children.
• What is the main cause of obesity, and why is it increasing with every passing day?
• Schools and colleges should work harder to develop methodologies to decrease childhood obesity.
• The government should not allow schools and colleges to include sweet or fatty snacks as a part of their lunch.
• If a mother is obese, can it affect the health of the child?
• Children who gain weight frequently can develop chronic diseases.

Obesity Argumentative Essay Topics

Do you want to write an argumentative essay on the topic of obesity?

The following list can help you with that!

Here are some examples you can choose from for your argumentative essay about obesity:

• Can vegetables and fruits decrease the chances of obesity?
• Should you go for surgery to overcome obesity?
• Are there any harmful side effects?
• Can obesity be related to the mental condition of an individual?
• Are parents responsible for controlling obesity in childhood?
• What are the most effective measures to prevent the increase in the obesity rate?
• Why is the obesity rate increasing in the United States?
• Can the lifestyle of a person be a cause of obesity?
• Does the economic situation of a country affect the obesity rate?
• How is obesity considered an international health issue?
• Can technology and gadgets affect obesity rates?
• What can be the possible reasons for obesity in a school?
• How can we address the issue of obesity?
• Is obesity a chronic disease?
• Is obesity a major cause of heart attacks?
• Are the junk food chains causing an increase in obesity?
• Do nutritional programs help in reducing the obesity rate?
• How can the right type of diet help with obesity?
• Why should we encourage sports activities in schools and colleges?
• Can obesity affect a person’s behavior?

Health Related Topics for Research Paper

If you are writing a research paper, you can explain the cause and effect of obesity.

Here are a few topics that link to the cause and effects of obesity.Review the literature of previous articles related to obesity. Describe the ideas presented in the previous papers.

• Can family history cause obesity in future generations?
• Can we predict obesity through genetic testing?
• What is the cause of the increasing obesity rate?
• Do you think the increase in fast-food restaurants is a cause of the rising obesity rate?
• Is the ratio of obese women greater than obese men?
• Why are women more prone to be obese as compared to men?
• Stress can be a cause of obesity. Mention the reasons how mental health can be related to physical health.
• Is urban life a cause of the increasing obesity rate?
• People from cities are prone to be obese as compared to people from the countryside.
• How obesity affects the life expectancy of people? What are possible solutions to decrease the obesity rate?
• Do family eating habits affect or trigger obesity?
• How do eating habits affect the health of an individual?
• How can obesity affect the future of a child?
• Obese children are more prone to get bullied in high school and college.
• Why should schools encourage more sports and exercise for children?

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Topics for Essay on Obesity as a Problem

Do you think a rise in obesity rate can affect the economy of a country?

Here are some topics for your assistance regarding your economics related obesity essay.

• Does socioeconomic status affect the possibility of obesity in an individual?
• Analyze the film and write a review on “Fed Up” – an obesity epidemic.
• Share your reviews on the movie “The Weight of The Nation.”
• Should we increase the prices of fast food and decrease the prices of fruits and vegetables to decrease obesity?
• Do you think healthy food prices can be a cause of obesity?
• Describe what measures other countries have taken in order to control obesity?
• The government should play an important role in controlling obesity. What precautions should they take?
• Do you think obesity can be one of the reasons children get bullied?
• Do obese people experience any sort of discrimination or inappropriate behavior due to their weight?
• Are there any legal protections for people who suffer from discrimination due to their weight?
• Which communities have a higher percentage of obesity in the United States?
• Discuss the side effects of the fast-food industry and their advertisements on children.
• Describe how the increasing obesity rate has affected the economic condition of the United States.
• What is the current percentage of obesity all over the world? Is the obesity rate increasing with every passing day?
• Why is the obesity rate higher in the United States as compared to other countries?
• Do Asians have a greater percentage of obese people as compared to Europe?
• Does the cultural difference affect the eating habits of an individual?
• Obesity and body shaming.
• Why is a skinny body considered to be ideal? Is it an effective way to reduce the obesity rate?

Obesity Solution Essay Topics

With all the developments in medicine and technology, we still don’t have exact measures to treat obesity.

Here are some insights you can discuss in your essay:

• How do obese people suffer from metabolic complications?
• Describe the fat distribution in obese people.
• Is type 2 diabetes related to obesity?
• Are obese people more prone to suffer from diabetes in the future?
• How are cardiac diseases related to obesity?
• Can obesity affect a woman’s childbearing time phase?
• Describe the digestive diseases related to obesity.
• Obesity may be genetic.
• Obesity can cause a higher risk of suffering a heart attack.
• What are the causes of obesity? What health problems can be caused if an individual suffers from obesity?
• What are the side effects of surgery to overcome obesity?
• Which drugs are effective when it comes to the treatment of obesity?
• Is there a difference between being obese and overweight?
• Can obesity affect the sociological perspective of an individual?
• Explain how an obesity treatment works.
• How can the government help people to lose weight and improve public health?

Writing an essay is a challenging yet rewarding task. All you need is to be organized and clear when it comes to academic writing.

• Choose a topic you would like to write on.
• Organize your thoughts.
• Pen down your ideas.
• Compose a perfect essay that will help you ace your subject.
• Proofread and revise your paper.

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The Role of Obesity as a Cardiac Disease Risk Factor in Patients with Type 2 Diabetes

• Cardiometabolic Disease (DM and CV) (CJ Lavie, Section Editor)
• Published: 05 September 2024

Cite this article

• Sushant Koirala 1 ,
• Michael Sunnaa 1 ,
• Thomas Bernier 2 &
• Ahmet Afsin Oktay 2  

Purpose of Review

Cardiovascular disease (CVD) is the leading cause of death globally and is closely associated with obesity and type 2 diabetes mellitus (T2DM). This review examines the interplay between obesity, T2DM, and CVD, highlighting the increasing prevalence and economic burden of these conditions.

Recent Findings

Pharmacologic therapies, particularly glucagon-like peptide-1 receptor agonists, show promise in substantial weight loss and subsequent reduction of adverse cardiovascular events in obese individuals with and without diabetes.

Obesity significantly contributes to the development of insulin resistance and T2DM, further escalating CVD risk. The common co-occurrence of these three conditions may involve several other pathophysiological mechanisms, such as chronic inflammation, increased visceral adiposity, and endothelial dysfunction. Until recently, lifestyle modifications and bariatric surgery had been the primary methods for weight loss and mitigating obesity-associated cardiovascular risk. Newer pharmacological options have led to a paradigm shift in our approach to obesity management as they provide substantial benefits in weight loss, glycemic control, and cardiovascular risk reduction.

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Obesity Management in Cardiometabolic Disease: State of the Art

Cardiovascular Complications of Obesity

Cardiovascular risk in diabetes mellitus: epidemiology, assessment and prevention

Data availability.

No datasets were generated or analysed during the current study.

Abbreviations

American Diabetes Association

• Cardiovascular disease

Cardiovascular outcome trial

Glucose-dependent insulinotropic polypeptide

Hemoglobin A1c

Heart failure

Heart failure with preserved ejection fraction

Glucagon-like peptide-1

• Glucagon-like peptide-1 receptor agonist

Major adverse cardiac event

Randomized controlled trial

Sodium glucose cotransporter-2

Sodium-glucose co-transporter-2 inhibitor

ST-elevation myocardial infarction

Type 2 Diabetes Mellitus

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Koirala, S., Sunnaa, M., Bernier, T. et al. The Role of Obesity as a Cardiac Disease Risk Factor in Patients with Type 2 Diabetes. Curr Cardiol Rep (2024). https://doi.org/10.1007/s11886-024-02129-z

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Home — Essay Samples — Nursing & Health — Public Health Issues — Obesity

Essay Examples on Obesity

Hook examples for obesity essays, "the silent epidemic among us" hook.

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"Obesity is a public health crisis with wide-ranging effects. Investigate the strain on healthcare systems, the rise of related diseases, and the economic impact of obesity."

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"Examine how cultural factors, including dietary habits, technology use, and sedentary lifestyles, have contributed to the obesity epidemic. What can we learn from these trends?"

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"Prevention is key to combating obesity. Discuss effective strategies for preventing obesity in children and adults, from education to policy changes."

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"In the midst of the obesity crisis, the body positivity movement is gaining ground. Discuss the importance of promoting self-acceptance and diverse body images."

Obesity in America: a Growing Epidemic

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Obesity as a Stigma Or a Threat to Health

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Obesity is a condition in which excess body fat has accumulated to such an extent that it may have a negative effect on health. Medical organizations tend to classify people as obese based on body mass index (BMI) – a ratio of a person's weight in kilograms to the square of their height in meters.

There are three types of obesity: Class 1 (low-risk) obesity, if BMI is 30.0 to 34.9; Class 2 (moderate-risk) obesity, if BMI is 35.0 to 39.9; Class 3 (high-risk) obesity, if BMI is equal to or greater than 40.0.

The major contributors to obesity are: diet, sedentary lifestyle, genetics, other illnesses, social determinants, gut bacteria, and other factors.

Excessive body weight has a strong link to many diseases and conditions, particularly cardiovascular diseases, diabetes mellitus type 2, obstructive sleep apnea, certain types of cancer, osteoarthritis, and asthma. As a result, obesity has been found to reduce life expectancy.

Most of the world's population live in countries where overweight and obesity kills more people than underweight. 39 million children under the age of 5 were overweight or obese in 2020. Worldwide obesity has nearly tripled since 1975. From 1999-2000 through 2017-March 2020, US obesity prevalence increased from 30.5% to 41.9%.

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The Role of Obesity in Type 2 Diabetes Mellitus—An Overview

Preethi chandrasekaran.

1 UT Southwestern Medical Center Dallas, 5323 Harry Hines Blvd. ND10.504, Dallas, TX 75390-9014, USA

Ralf Weiskirchen

2 Institute of Molecular Pathobiochemistry, Experimental Gene Therapy and Clinical Chemistry (IFMPEGKC), Rheinisch-Westfälische Technische Hochschule (RWTH), University Hospital Aachen, D-52074 Aachen, Germany

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This review only presents data that were previously published. No new data was generated.

Obesity or excessive weight gain is identified as the most important and significant risk factor in the development and progression of type 2 diabetes mellitus (DM) in all age groups. It has reached pandemic dimensions, making the treatment of obesity crucial in the prevention and management of type 2 DM worldwide. Multiple clinical studies have demonstrated that moderate and sustained weight loss can improve blood glucose levels, insulin action and reduce the need for diabetic medications. A combined approach of diet, exercise and lifestyle modifications can successfully reduce obesity and subsequently ameliorate the ill effects and deadly complications of DM. This approach also helps largely in the prevention, control and remission of DM. Obesity and DM are chronic diseases that are increasing globally, requiring new approaches to manage and prevent diabetes in obese individuals. Therefore, it is essential to understand the mechanistic link between the two and design a comprehensive approach to increase life expectancy and improve the quality of life in patients with type 2 DM and obesity. This literature review provides explicit information on the clinical definitions of obesity and type 2 DM, the incidence and prevalence of type 2 DM in obese individuals, the indispensable role of obesity in the pathophysiology of type 2 DM and their mechanistic link. It also discusses clinical studies and outlines the recent management approaches for the treatment of these associated conditions. Additionally, in vivo studies on obesity and type 2 DM are discussed here as they pave the way for more rigorous development of therapeutic approaches.

1. Introduction

The rapid development of global urbanization and modernization has lasting effects on lifestyle aspects such as unhealthy eating habits, lack of exercise, increased stress and environmental factors. These factors contribute to the alarming growth of obesity and type 2 DM worldwide. Obese individuals develop insulin resistance, which is characterized by impaired insulin action in the liver and reduced glucose uptake in fat and muscle [ 1 ]. While lifestyle changes and medications are recommended for prevention, they have not been successful in suppressing the increasing incidence conditions. Therefore, it is crucial to gain a deeper understanding of the molecular mechanisms linking obesity and type 2 DM in order to address this global healthcare challenge effectively.

The intricate connections and sharing of pathophysiological mechanisms between obesity and type 2 DM amplify the prevalence and incidence of insulin resistance, dyslipidemia, NAFLD and a constellation of metabolic abnormalities in obese individuals. Increased body mass index (BMI) and abdominal fat distribution linearly increases the risk of type 2 DM due to alterations in adipose tissue biology that links obesity with insulin resistance and beta cell dysfunction [ 1 ]. Abdominal obesity, commonly determined by waist-to-hip ratio, is an independent factor for the development of hypertension and elevated fasting glucose, even if the overweight individual with predominant abdominal fat does not meet the BMI criteria for obesity [ 2 ]. Multiple in vivo and clinical studies have demonstrated a cause-and-effect relationship between obesity and type 2 DM, unraveling their intimate connections. It is shocking to note that according to the WHO fact sheet, at least 41 million children under the age 5 are overweight or obese (BMI ≥ 35 kg/m 2 ) as of 2016. If this trend continues, 60% of the world’s population will be obese or overweight by 2030 [ 3 ]. According to WHO, obesity accounts for 44% of diabetes and the incidence of obesity-related diabetes is expected to double to 300 million by 2025 [ 4 ].

It is interesting to note that during starvation, adipose tissue, which serves as a major fuel reserve, provides a critical energy source for survival. Additionally, adipose tissue modifies various physiological functions, including appetite, reproduction and insulin action, through the secretion of adipokines and exosomes [ 1 ]. In obese individuals, non-esterified fatty acids play a crucial role in the development of insulin resistance and beta cell dysfunction [ 1 ].

The close relationship between obesity and diabetes has led to the term “diabesity”, which highlights that the majority of individuals with diabetes are obese or overweight [ 5 ]. While type 2 DM is influenced by genetic predisposition and ethnicity which are non-modifiable risk factors, it can still be prevented or managed by addressing modifiable risk factors such as obesity. Despite recent advancement in management strategies, obesity and diabetes remain a significant interconnected public health challenge worldwide. In this review, we will explore the mechanistic link between obesity and diabetes, discuss clinical and in vivo studies that focus on this association and briefly touch upon the clinical definitions of obesity, diabetes and epidemiology.

2. Definitions and Epidemiology of Obesity and Type 2 DM

Obesity is defined as the excessive accumulation of fat in various parts of the body or organs, known as ectopic fat or throughout the body. It is a chronic, progressive, relapsing condition with multiple factors that lead to adverse metabolic and psychosocial health consequences [ 6 ]. One of the main causes of obesity is an imbalance between the excess energy stored and the energy utilized by the body, which can disrupt nutrient signals and result in insufficient energy expenditure [ 6 ]. Assessing the risk factors for adiposity involves measuring height, weight, BMI, waist circumference and body fat percentage. The diagnosis of obesity relies on the BMI cut off and the relationship between body weight, fat distribution pattern and visceral fat [ 7 ]. BMI alone is no longer sufficient to evaluate obesity, as it is a diverse condition. Table 1 displays the classification of obesity based on BMI and waist circumference [ 7 ].

Classification of obesity based on body mass index and waist circumferences.

The anthropometric assessment of percentage body fat is a more accurate measure of adiposity than BMI [ 8 ]. The Obesity Medicine Association classification of percentage body fat is shown in Table 2 [ 8 ].

Anthropometric assessment of body fat percentage as a measure of adiposity.

It is interesting to note that by 2030, an estimated 14% of men and 20% of women in the world’s total population will develop clinical obesity. Additionally, it is estimated that 18% of individuals will have a BMI greater 30 kg/m 2 , 6% will have a BMI greater than 35 kg/m 2 , and 2% will have a BMI greater than 40 kg/m 2 [ 9 ]. According to the World Obesity Federation, countries with high socioeconomic status and per capita income are at a greater risk of experiencing an increased prevalence of obesity [ 9 ]. It is alarming to note that approximately two-thirds of the adult population in the United States is either obese or overweight [ 10 ].

The prevalence of obesity in the United States has alarmingly increased over the past decade. According to published data from 2017 to 2020, 42.4% of adults have a BMI ≥ 30 kg/m 2 , while 20.9% of youth have a BMI ≥ 30 kg/m 2 . Additionally, the age-adjusted prevalence of severe obesity, defined as BMI ≥ 40 kg/m 2 , is 9.2% [ 11 ].

Currently, only around 30% of the adult population in the US has a normal BMI between 18–25 kg/m 2 [ 12 ]. When considering race and ethnicity, the highest rates of obesity are found among black women, Native Americans and Hispanics [ 13 ]. It is projected that by 2023, approximately 50% of the US adult population will be obese with around 25% developing severe obesity [ 14 ].

From a global perspective, the obese population worldwide has risen steadily over the past few decades with a six-fold increase in adults with obesity between 1975 and 2016. This increase is driven by socioeconomic advances, which pose a significant healthcare burden and contribute to the rise in mortality complications associated with obesity, such as DM and cardiovascular diseases [ 15 ].

Obesity plays an inevitable role in the increased prevalence of type 2 DM, a chronic condition where the body fails to produce sufficient insulin or cannot efficiently utilize insulin resulting in elevated blood glucose levels as its primary manifestation. Type 2 DM is characterized by low insulin secretions from β-cells and peripheral insulin resistance, leading to elevated levels of fatty acids. This causes a decrease in glucose transport into muscle cells, increased fat breakdown and hepatic glucose production [ 16 ].

This is the fastest-growing pandemic and health emergency globally. According to the latest estimates by the International Diabetes Federation, the number of diagnosed cases of DM is predicted to reach 643 million by 2030 and 783 million by 2045 [ 17 ]. Additionally, the majority of undiagnosed type 2 DM cases are concentrated in Africa, Southeast Asia and the Western Pacific. In 2021, there were 541 million adults diagnosed with impaired glucose tolerance and 319 million adults with impaired fasting glucose. These numbers are predicted to increase to 730 million and 441 million, respectively, by 2045 [ 17 ].

Previous studies have shown that the relative risk of developing type 2 DM is 4.6-fold higher for woman and 3.5-fold higher for men with a BMI greater than 29.9 kg/m 2 compared to their same-sex peers with a BMI less than 24.9 kg/m 2 [ 18 ]. It is important to note that the associations between central obesity and comorbidities vary among different races and ethnicities ( Figure 1 ).

Prevalence of type 2 diabetes mellitus (in 2019), obesity (in 2016) and overweight (in 2016) in selected countries. This figure has been redrawn in a modified form from [ 19 ].

For instance, in Asian populations with type 2 DM, central obesity is a more accurate predictor than BMI [ 20 ]. Interestingly, for individuals of European ancestry, the thresholds for central obesity are determined by a waist circumference greater than 94 cm (37 inches) for men and greater than 80 cm (31.5 inches) for women. These thresholds for individuals of South Asian, Chinese and Japanese origin are greater than 90 cm (35.5 inches) for men and greater than 80 cm (31.5 inches) for women [ 21 , 22 ].

Diabetes is a chronic metabolic disorder with multiple causes, characterized by consistently high blood glucose levels due to defects in insulin secretion, action or both. Type 2 DM is more common than type 1 DM, accounting for 90–95% cases. It is strongly influenced by genetics and involves resistance to insulin action and inadequate compensatory insulin secretion [ 23 ]. Most patients with type 2 DM are obese, with a higher percentage of body fat or abnormal distribution, which is related to the pathophysiology of DM. Adipose tissue promotes insulin resistance by releasing more free fatty acids [ 24 ]. Other contributing factors include peripheral insulin resistance, dysregulation of hepatic glucose production, decreased beta cell function and beta cell failure [ 1 ].

The diagnosis of type 2 DM is made when the patient meets one of the following criteria: glycated hemoglobin (HbA1 C ) ≥ 6.5%, fasting blood glucose ≥ 126 mg/dL or 2-h post-prandial glucose ≥ 200 mg/dL. Diabetes-related morbidity and complications can be substantially reduced with tight glycemic control, aiming for an HbA1c of less than 7% [ 25 ].

According to the International Diabetes Federation (IDF), 415 million adults aged 20–79 years were diagnosed with DM in 2015 and the number of people suffering from diabetes increase in that group rose to about 573 million adults in 2021 ( Figure 2 ).

Prevalence of diabetes worldwide in 2021. A total of 573 million people suffered from diabetes in 2021. The figure has been redrawn and modified based on information from [ 26 ].

The global population with DM is predicted to increase to another 200 million by 2040 [ 27 ]. In the United States, Native Americans, Hispanics and Asian Americans are the most affected population by type 2 DM [ 28 ]. It is estimated that 70% of individuals with pre-diabetes will eventually develop type 2 DM by 2030 [ 27 ].

Interestingly, certain regions such as Fiji and American Samoa have reported the highest prevalence of the disease. Southeast Asian countries have also seen an increase in the last two decades. The top spots with the greatest total number of individuals with type 2 DM include China (88.5 million), India (65.9 million) and the US (28.9 million), which can be attributed to their large population size [ 29 ].

3. Mechanistic Link

3.1. white and brown adipose tissue.

It is crucial to understand the difference between classifications and subsets of adipose tissue. Morphologically, adipose tissue can be classified as white adipose tissue (WAT) or brown adipose tissue (BAT). WAT can be further divided into two subsets: subcutaneous adipose tissue and visceral adipose tissue. Subcutaneous adipose tissue is characterized by small adipocytes that exhibit stronger anti-lipolytic effects of insulin. On the other hand, visceral adipose tissue is characterized by larger adipocytes and is metabolically very active. In healthy lean individuals, the WAT mass is confined to specific depots. However, in cases of obesity, the WAT mass increases ectopically in areas such as mesenteric, omental or retroperitoneal fat [ 30 , 31 ].

Brown fat, which comprises 1–2% of total fat stores, functions by generating heat through the uncoupling of the respiratory chain. This allows for the fast production of ATP through oxidative phosphorylation. This process helps clear plasma triglycerides and prevents the storage of excess fat in other areas of the body. Brown fat also acts as a reservoir for excess blood glucose and free fatty acids, aiding their disposal. Non-shivering thermogenesis, mediated by UCP1 in BAT, is considered a promising way for increasing energy expenditure. The differentiation of resident progenitor cells into mature adipocytes is facilitated by critical factors such as BMP7 and EBF2, leading to the development of a beige pre-adipocyte phenotype. This is followed by the transcriptional activation of UCP-1, PRDM16 and Zfp516. A crucial step in this differentiation process involves the deacetylation of PPARγ by SIRT1 and the promotion of mitochondrial biogenesis. Additionally, the browning machinery also involves PGC-1α and C/EBPs [ 32 ].

Numerous studies have shown that dysfunction in BAT contributes to insulin resistance and hyperlipidemia. Multiple rodent studies have demonstrated that transplanted BAT improves glucose tolerance, insulin sensitivity and reduces obesity. Furthermore, it has been found that fibroblast growth factor 21 (FGF21) stimulates the browning of WAT, activating brown adipocytes and inducing thermogenesis. A clinical trial involving LY2405319, a variant of FGF21, in obese individuals with type 2 DM showed improved body weights, decreased triglyceride levels and improved insulin sensitivity [ 33 ].

The role of macrophages in eliciting metabolic inflammation and their interactions with adipose cells have been well-known in obesity-associated insulin resistance for years. Interestingly, the number of macrophages in brown fat depots is reported to be low, suggesting that BAT has an inherent ability to reduce the inflammatory capacity of macrophages compared to WAT, enhancing this profile. Therefore, it is evident that the activation of brown adipose tissue in WAT-mediated thermogenic activity counteracts insulin resistance and metabolic dysfunction [ 34 ].

3.2. Adipogenesis and Healthy Adipose Tissue

PPARγ is the master regulator of adipogenesis and the maintenance of differentiation from pre-adipocytes to mature adipocytes. It is important to note that other factors such as C/EBPs, KLFs, PRDM16 and PGC-1α are also involved in this regulation. PPARγ upregulates the expression of C/EBPα by promoting its transcription, which, in turn, is associated with elevated expression of other adipogenic genes. PRDM16 functions to suppress white adipocyte specific genes by forming complexes with terminal binding proteins CTBP1 and CTBP2. The activation of brown fat-specific genes occurs when CTBPs are displaced through the recruitment of PPARγ co-activators PGC-1α and PGC-1β [ 35 , 36 ].

PGC-1α, a master transcriptional cofactor for mitochondrial biogenesis, is mainly expressed in BAT. One of the main downstream mediators of PGC-1α is the transcription factor A mitochondria (TFAM), which coats and stabilizes individual mtDNA inducing promoter activity. Furthermore, PGC-1α is involved in the response to oxidative stress by inducting SIRT3, which plays a critical role in β-oxidation and anti-oxidative reactions by modulating acetylation levels of mitochondrial enzymes. The crosstalk between adipogenesis and mitochondrial biogenesis confirms the involvement of PGC-1α in obesity-linked insulin resistance, as it is widely accepted as a marker of transdifferentiation of white into brown adipocytes [ 37 , 38 ].

Recently, multiple studies have shed light on the central role of HO-1 in maintaining beige-like adipose tissue and improving liver functions and insulin sensitivity. HO-1 protects against obesity-induced insulin resistance through the degradation of pro-oxidant heme and the production of carbon monoxide and bilirubin, which have anti-inflammatory properties. As a result of obesity, the levels of reactive oxygen species (ROS) within the adipocytes increase, leading to repression of HO-1 and SOD. This, in turn, increases the production of pro-inflammatory cytokines. Recent research has shown that HO-1 in adipocytes can reverse the detrimental effects of obesity, including insulin resistance and dyslipidemia [ 39 , 40 ].

3.3. Dysfunctional Adipogenesis

Adipose tissue is the major reservoir for storing or releasing lipids, depending on fuel availability. Impairment in the pathways associated with the differentiation and proliferation of precursor cells into adipose cells leads to impaired adipogenesis and reduced ability to store excess lipids. This subsequently leads to insulin resistance due to the accumulation of ectopic fat. Multiple studies suggest that BMP4 signaling is important for the recruitment and differentiation of adipocytes and the development of a brown phenotype, which protects against obesity and obesity-linked insulin resistance. Dysregulation of BMP4 signaling can lead to adipocyte hypertrophy and systemic metabolic dysfunction [ 41 ].

The multi-dimensional contributions to insulin resistance such as specific nutrients, growth factors, a high-calorie diet and incretin, play a significant role in the development of type 2 DM ( Figure 3 ) [ 42 ].

Multifactorial pathophysiology of obesity and type 2 diabetes. Genetic and epigenetic factors, along with an unhealthy lifestyle play significant roles in the development of both obesity and type 2 diabetes. Various factors, including adipokines, pro-inflammatory cytokines, non-esterified fatty acids (NEFA) and others contribute to visceral fat accumulation, β-cell dysfunction, changes in gut microbiota and gut barrier leakage. In addition, inflammatory reactions in the hypothalamus might contribute to the onset of diabetes and vice versa. Diabetes impacts energy homeostasis and hyper-activates regulatory neurons as well as the surrounding microglia in the hypothalamus.

3.4. Adipose Tissue Dysfunction and Inflammation

As previously mentioned, adipose tissue is highly flexible and can adapt to rapid changes in energy balance during periods of fasting and feeding. However, if this adaptive response is altered, it can lead to the development of metabolic dysfunction in people with obesity [ 43 ]. Numerous in vivo studies have revealed a variety of complex biological and physiological processes in adipose tissue that contribute to insulin resistance. In particular, adipose tissue produces numerous adipokines such as adiponectin, leptin, visfatin, resistin, apelin, omentin, retinol binding protein (RBP4), vaspin and many others that impact the overall activity of different organs including the liver, pancreas, gut, brain and skeletal muscle ( Figure 4 ).

Adipokines released by adipose tissue are central in the control of endocrine and secretory functions of many organs. The adipose tissue secretes various molecules known as adipokines which act as powerful signal molecules. The activity of these adipokines impacts biological processes in liver, pancreas, gut, brain, skeletal muscles and many other organs.

These processes include adipocyte hypoxia, which is caused by increased oxygen demand and stimulates fibrogenesis and macrophage chemotaxis. This leads to an increase in branched chain amino acids concentration in the plasma, an increase in the number of adipocyte macrophages and T cells, a decrease in adipose tissue production and adiponectin (an insulin sensitizing hormone), an increase in lipolytic activity of adipose tissue leading to the release of free fatty acids into circulation and alterations of exosomes derived from adipose tissue macrophages [ 44 , 45 , 46 , 47 , 48 ]. Among these factors, it has been proposed that adipose tissue inflammation is the main driving force behind insulin resistance in obese individuals [ 49 ]. Adipocyte hypoxia occurs because of the activation of saturated FFA stimulated adenine nucleotide translocase 2 (ANT2), an inner mitochondrial protein that is triggered by a high fat diet and obesity.

This exacerbates dysfunction and inflammation in adipose tissue, causing activated macrophages and hypertrophied adipocytes to increase the levels of pro-inflammatory cytokines such as TNF-α, IL-1β, monocyte chemoattractant protein-1 (MCP-1) and IL-6, which ultimately leads to the development of metabolic inflammation [ 50 ]. This chronic inflammatory state is a key factor contributing to the pathogenesis of insulin resistance, which decreases the glucose uptake in muscle, leads to increase glucose production in liver, provokes β-cell dysfunction in pancreas and results in endocrine dysfunction of adipose tissue ( Figure 5 ).

Pro-inflammatory cytokines in the pathogenesis of metabolic inflammation and insulin resistance. In the development of insulin resistance and type 2 diabetes, several cytokines such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), monocyte chemoattractant protein-1 (MCP-1), IL-6 and others released by activated tissue macrophages and by adipocytes play a significant role. These pro-inflammatory molecules provoke important responses in liver, skeletal muscle, fat tissue and pancreas, resulting in endocrine dysfunction, impaired glucose disposal, impaired β-cell function and reduced suppression of glucose production. The abbreviations used are as follows: AKT, protein kinase B; IRS, insulin receptor substrate; PKCζ, protein kinase Cζ; PKC𝜃, protein kinase C𝜃; PP2A, protein phosphatase 2A.

Adipose tissue macrophages also play a causative role in obesity-associated insulin resistance. Recent studies have shown that decreased macrophage recruitment in obesity can alleviate insulin resistance in animal models [ 51 ].

Few studies have deciphered the role of toll-like receptors in inflammation-associated insulin resistance in obesity. For example, one study revealed that the abolition of TLR4 alleviated obesity-induced insulin resistance through reducing oxidative stress by metabolic reprogramming of mitochondria in visceral fat [ 52 ].

The signaling pathways involved in the inflammatory mechanisms include the activation of JNK1 by TNF-α, which lead to serine phosphorylation of insulin receptor substrate 1 (IRS1) and impairs the action of insulin [ 53 ]. Other inflammatory mediators attributed to obesity-induced insulin resistance belong to the class of suppressor of cytokine signaling (SOCS) proteins. These proteins function as part of a feedback pathway in cytokine signaling. The inhibition of insulin signaling by cytokines occurs through interference with the tyrosine phosphorylation of either IRS1 or IRS2 [ 54 ].

It is well known that adipose tissue maintains whole-body energy homeostasis. Obesity, which occurs due to the accumulation of WAT in visceral organs, leads to a lack of angiogenesis in subcutaneous adipose tissue. This results in an inability to store excess energy, leading to insulin resistance in obese individuals. Therefore, there may be a connection between adipose tissue angiogenesis, vascular function and insulin sensitivity. A study supported this idea by showing improved metabolic homeostasis in mice when capillary-derived beige adipocytes were implanted [ 55 ].

3.5. Adiponectin

An important biomarker of adipose tissue health is plasma adiponectin, which is directly associated with insulin sensitivity and has an inverse relationship with the percentage of body fat [ 56 ]. Adiponectin has a variety of functions, including anti-inflammatory, anti-fibrotic and insulin-sensitizing effects. These effects are partly mediated by increased ceramidase activity and decreasing intracellular ceramide levels. Adiponectin levels are low in obesity [ 57 ]. In the liver, adiponectin decreases the influx of fatty acids, increases fatty acid oxidation and reduces hepatic glucose output. In the muscle, adiponectin stimulates fatty acid oxidation through AMP-activated protein kinase. Although the release of free fatty acids from visceral fat was previously believed to cause insulin resistance, it is unlikely to be a major factor since only 20% of the free fatty acids are derived from the lipolysis of visceral fat [ 58 ].

3.6. Other Adipokines and Cortisol

Plasminogen activator inhibitor-1 (PAI-1), a member of the serine protease inhibitor family, is elevated in obesity and insulin resistance and predicts the risk of type 2 DM [ 59 ]. IL-6 levels predict the development of DM, and when administered peripherally in mice, Il-6 induces hyperglycemia, hyperlipidemia and insulin resistance by the downregulating of IRS and the upregulating of SOCS-3 [ 60 ]. Cortisol causes insulin resistance and type 2 DM by opposing the anti-gluconeogenic effects of insulin in the liver [ 61 ].

3.7. Lipids and Free Fatty Acids

The contribution of increased gluconeogenesis in obese individuals causes fasting and postprandial hyperglycemia. This is because these individuals have an impaired insulin ability to suppress hepatic glucose production. The increase in hepatic gluconeogenesis is due to impaired suppression of adipose tissue lipolysis, which increases the delivery of free fatty acids to the liver [ 62 ]. Defective AKT activation promotes the activation of lipolytic enzymes, which impairs GLUT4 translocation to the membrane and worsens hyperglycemia [ 63 ].

In obese individuals, the increased lipid oxidation causes a high concentration of plasma-free fatty acids, which leads to insulin resistance. This ‘lipid overflow’ limits the oxidation of glucose and, as a result, in skeletal muscle, the preference for using free fatty acids as an energy source inhibits glycogen synthase and restricts the use of glucose from glycogen stores. Consequently, there is a compensatory increase in plasma glucose and insulin levels over time. However, despite this compensatory effect, there is still resistance to glucose uptake, resulting in type 2 DM ( Figure 6 ) [ 64 ].

Fats and lipids in the pathogenesis of type 2 diabetes. An overabundance of fatty acids and lipids, resulting from a high-caloric diet enriched in fat (which cannot be stored in adipocytes), lead to increased levels of circulating fat that accumulate in peripheral tissues such as the liver, muscles and pancreas. This accumulation triggers numerous molecular changes that result in increased glucose production, lowered glucose disposal and impaired insulin secretion. These factors are hallmarks of diabetes. This figure was adapted in a modified form from [ 65 ].

Previously, it was hypothesized that the competition between increased circulating fatty acids and glucose for oxidative metabolism in insulin responsive cells explained the association between obesity and type 2 DM [ 66 ]. However, more recent research suggests that glucose uptake is the rate-limiting step in fatty acid-induced insulin resistance rather than intracellular glucose metabolism [ 67 ]. According to this model, fatty acids, along with metabolites such as acyl-CoA, ceramides and diacylglycerols, serve as signaling molecules that activate protein kinases. These protein kinases impair insulin signaling by increasing the serine phosphorylation of insulin receptor substrate which are key mediators of insulin receptor signaling [ 67 ].

3.8. Distribution of Fat and Ectopic Fat Storage

A striking feature in determining the risk of adiposity induced type 2 DM is the distribution pattern of fat throughout the body. For example, obese individuals with abdominal subcutaneous, intraabdominal fat, intrahepatic triglycerides and pancreatic fat are at a higher risk of developing type 2 DM compared to people with lower body fat accumulation [ 68 ]. The role of intramyocellular lipids (IMCL) is increasingly recognized as an important factor in modulating insulin action. Several transgenic animal models have demonstrated that decreased IMCL improves insulin sensitivity [ 69 ]. The accumulation of IMCL in obese patients is due to increased levels of lipid peroxidation and the production of lipid peroxidation byproducts such as 4-hydroxynonenal (4-HNE) as well as decreased muscle fatty acid beta oxidation which affects insulin sensitivity [ 70 ].

Ectopic lipid accumulation has been implicated in insulin resistance due to the activation of reactive oxygen species (ROS), mitochondrial dysfunction or endoplasmic reticulum (ER) stress [ 71 ]. The persistent imbalance between the production of ROS and antioxidants is the main cause of oxidative stress, leading to fat accumulation in both humans and mice [ 72 ]. The increase in ROS in pre-diabetes is caused by an increase in fatty acids which results in oxidative stress due to increased mitochondrial uncoupling and beta oxidation subsequently, leading to increased ROS production [ 73 ]. Multiple in vitro studies have elucidated that ROS and oxidative stress activate potential targets of the insulin-signaling pathway such as the insulin receptor and IRS proteins [ 74 ]. In insulin resistance, ectopic fat accumulation is associated with decreased mitochondrial oxidative activity and ATP synthesis. The accumulation of intramyocellular fat is attributed to decreases in muscle mitochondria due to decreased expression of PPARγ and PGC-1β, which regulate mitochondrial biogenesis [ 75 ].

A possible mechanism for the generation of excess ROS is the excessive formation of superoxide by NADPH oxidase (NOX). This inactivates the critical metabolic enzymes, initiating lipid peroxidation in obesity. The excessive production of ROS activates numerous pro-inflammatory cytokines including NF-κB, which promotes insulin resistance. The dysregulation or ROS causes disturbances in multiple biochemical mechanisms such as oxidative phosphorylation, the generation of superoxide from NOX, PKC activation and hyperleptinemia. Additionally, the activation of serine kinases by ROS results in hyperphosphorylation of serine/threonine, inhibiting the tyrosine phosphorylation of IRS1 and IRS2 thereby diminishing insulin signaling [ 76 ].

In the case of lipotoxicity, the normal dynamics of mitochondria are altered, damaging mitochondrial DNA and increasing mitophagy, a process through which dysfunctional mitochondria are removed through lysosome fusion. This increase in mitophagy decreases the number of mitochondria, exacerbating lipid accumulation and lipotoxicity, which causes mitochondria-mediated cell apoptosis. Thus, mitochondrial dysfunction causes an overall alteration of metabolism, increased respiration and excessive acetyl CoA production. It is fascinating to note that the characteristics of mitochondria are also altered in obese states. This includes increased lipid peroxides, increased DAG and ceramides due to incomplete fatty acid oxidation. The combined effect of mitochondrial dysfunction and oxidative stress produces damage-associated molecular patterns that activate inflammatory signaling pathways such as TLR9-neutrophil-NF-κB pathways and NLRP3/Caspase 1/IL-1β pathways [ 77 ].

Another pathway implicated in insulin resistance is ER stress. One possibility for how obesity leads to ER stress is that ectopic lipid storage triggers ER stress through mechanical stress or disruptions in intracellular nutrient and energy fluxes, as well as changes in tissue architecture [ 78 ]. Strikingly, chronic overnutrition and obesity generate an excess of unfolded protein response transducers, which in turn leads to the release of pro-inflammatory cytokines. Ultimately, this process leads to the development of insulin resistance [ 79 ].

3.9. Disturbances in Lipid Homeostasis

Dyslipidemia is a hallmark feature of type 2 DM, characterized by increased levels of triglycerides, triglyceride-rich lipoproteins and decreased levels of high-density lipoproteins. Normally, chylomicrons deliver dietary lipids to the liver. Once in circulation, lipoprotein lipase, activated by apolipoprotein C-II, breaks down the triglycerides in the chylomicron core, releasing free fatty acids. As triglycerides are progressively removed, chylomicron remnants are formed and cleared by hepatocytes with the incorporation of apolipoprotein E (ApoE). This, along with the uptake of free fatty acids generated by lipolysis, is the main source of very low-density lipoproteins (VLDL) assembly and secretion. VLDL is gradually broken down to form smaller VLDL particles, and eventually low-density lipoproteins (LDL). However, in type 2 DM and insulin resistance, the efficient process of lipoprotein metabolism and clearance is impaired, leading to disruptions in the clearance of VLDL and chylomicrons [ 65 , 80 , 81 , 82 ].

4. In Vivo Models

Multiple in vivo studies have been conducted to shed light on the complex pathways that connect obesity and type 2 DM, which have the potential to be translated into clinical studies. A recent study found that PAI-1 levels were higher in obese individuals with insulin resistance compared to obese individuals without insulin resistance [ 83 ]. Additionally, a study using rodent models showed that overexpression of PAI-1 in adipocytes led to insulin resistance, while the knockout of PAI-1 in adipocytes improved insulin action [ 84 ].

Animal studies have demonstrated the importance of intramyocellular lipids in regulating insulin action. For example, the knockout of the fatty acid translocase CD36 resulted in improved insulin sensitivity and reduced fatty acid uptake, despite increased levels of plasma free fatty acids [ 85 ].

In another interesting study, a KK-Ay transgenic mouse model was developed to exhibit hyperglycemia, hyperinsulinemia and moderate obesity. The effect of Exendin 4, a GLP1-1 receptor agonist, was tested and shown to increase insulin secretion and reduce glucose levels [ 86 , 87 ].

The ob/ob mouse model, generated in 1949, is the most popular model for severe hyperglycemia and a monogenic model of obesity caused by a lack of leptin production. This model has been widely used in numerous studies. For instance, treatment with Sibutramine for six weeks in six-week-old ob/ob mice resulted in a 12% reduction in weight gain, decreased plasma insulin levels and improved insulin sensitivity [ 88 , 89 ].

Another commonly used obese rat model is the Zucker rat, in which the regulation of the leptin signal for reduced food intake is non-functional, resulting in preferential deposition of lipids in adipose tissue. By 14 weeks, these Zucker rats have a fat percentage of 40%. Although these animals exhibit insulin resistance and obesity, they are not overtly diabetic [ 90 , 91 ]. The effect of Sibutramine on these rats was examined, demonstrating a significant reduction in food intake [ 92 ]. A sub-strain of the Zucker rats, known as the Zucker diabetic fatty rats, has been widely utilized as an animal model to test various anti-diabetic and anti-obesity drugs. For instance, Liraglutide significantly attenuated the progression of diabetes in these rats, along with a reduction in blood glucose levels [ 93 ].

An important limitation of monogenic models deficient in leptin is that they do not accurately represent the pathogenesis of obesity in humans. Therefore, mouse and rat models induced by diet were developed to mimic human-like conditions. For instance, the C57BL6/J strain is commonly used to create a diet-induced obese model due to its propensity for obesity [ 94 ]. The commonly used rat strains for developing diet-induced obesity (DIO) models are Wistar, Sprague–Dawley, Long Evans, and Osborne Mendel rats [ 95 ]. In these DIO rats, Sibutramine and Liraglutide have shown effects on reducing body weight that are comparable to those in humans. However, the effects on plasma lipids and glucose tolerance still need to be further explored [ 96 ]. One major drawback of DIO rat models is that they often develop hyperinsulinemia instead of hyperglycemia. This has led to the development of a polygenic rat model that exhibits adult-onset obesity, insulin resistance and type 2 DM without the need for dietary intervention while maintaining leptin signaling [ 97 ].

One striking model is the development of UC Davis-type DM rats, in which Liraglutide (0.2 mg/kg) demonstrated a decrease in body weight and delayed or prevented the onset of diabetes. This treatment also led to a decrease in fasting plasma insulin levels and improved insulin sensitivity [ 98 , 99 ].

Another model, the New Zealand obese mouse (NZO) polygenic model crossed with non-obese nondiabetic (NON) mouse, resulted in NONcNZO10/LTJ mice. In these mice, it was shown that the selective β3 adrenergic receptor agonist CL316,243 reduced body weight and suppressed the development of diabetes [ 99 , 100 ].

A polygenic mouse model with moderate obesity and male-derived hyperglycemia is the Tallyho mouse model. The outcome of pharmacological interventions in these models remains unclear and needs further exploration [ 101 ]. Another interesting model is the gorringen minipig model, which also has limited information on pharmacological intervention studies. Liraglutide was shown to promote weight loss in these animals, in a similar method to human clinical obesity studies [ 102 ].

In an interesting study by Berg et al., it was demonstrated that administration of adiponectin improved insulin resistance in animal models [ 103 ]. Adiponectin-deficient mice developed glucose intolerance and insulin resistance. In contrast, adiponectin overexpression improved insulin sensitivity, glucose tolerance and reduced serum fatty acids.

Recent studies have demonstrated protection against obesity-induced insulin resistance through the overexpression of ER chaperones. In contrast, the knockdown of these chaperones had the opposite effect in mice [ 104 ].

5. Clinical Studies

Numerous clinical studies are ongoing on obesity and type 2 DM to strategize effective management and prevention. Although there are several valuable clinical studies, a few important and interesting studies are discussed here. More recently, a milestone discovery demonstrated that metabolically unhealthy obese individuals have a greater number of adipose tissue-derived exosomes compared to individuals with normal glucose tolerance and hepatic triglycerides [ 83 ].

Another interesting study demonstrated that lowering the levels of free fatty acids doubled the insulin sensitivity, increasing it from 25% to 50% of the normal values in obese individuals with type 2 DM [ 105 ]. Gastaldelli et al. elucidated that insulin resistance is directly proportional to visceral fat mass regardless of BMI [ 106 ]. In the same context, one study elucidates that body fat distribution is a crucial factor in the development of type 2 DM, independent of obesity stages. Also, individuals with insulin resistance were shown to have increased intramyocellular lipid content and decreased subcutaneous fat deposition [ 107 ]. A meta-analysis from the United States and Europe revealed that obese men have a 7-fold higher risk and obese women have a 12-fold higher chance of developing type 2 DM compared to those with normal weight [ 105 ]. The same study reported better glycemic control in type 2 DM patients on a weight loss regimen, highlighting the interdependent relationship between type 2 DM and obesity [ 108 ].

A fascinating randomized controlled trial of Semaglutide, specifically the 2-year STEP 5 trial, was conducted to test its long-term efficacy and safety in adults with obesity and type 2 DM. The participants achieved a weight loss of greater than 5% from the baseline at week 104, and also experienced improvements in diastolic blood pressure, HbA1c, fasting blood glucose, fasting serum insulin, total cholesterol, triglycerides, VLDL and LDL. This further confirms a meaningful correlation between obesity and type 2 DM as evidenced by improvements in both parameters [ 109 ]. A similar randomized clinical trial phase 3 was conducted on Tirzepatide, a glucose dependent insulinotropic polypeptide for 72 weeks on patients with obesity and type DM. The trial observed a weight reduction of 5% along with improvements in fasting insulin and lipid levels [ 110 ].

A meta-analysis on the outcome of HbA1c from lifestyle and weight loss interventions revealed that out of the 19 study groups with type 2 DM and obesity, 17 groups reported improvement in blood glucose, lipids and blood pressure over a 12-month period with a 5% reduction in weight from the baseline [ 111 ]. A significant finding was obtained in a diabetic prevention program, where moderate weight loss through lifestyle interventions in an obese population reduced the incidence of DM by 58%, whereas Metformin alone only reduced it by 31% [ 112 ].

In a retrospective study by Iglay et al., it was found that the most notable comorbid condition associated with type 2 DM is obesity (78.2%), followed by hyperlipidemia (77.2%). The highest co-prevalence was demonstrated for hypertension and hyperlipidemia (67.5%), followed by obesity and hyperlipidemia (62.5%) [ 113 ].

A study conducted by Gaich and colleagues tested the effects of fibroblast growth factor 21 (FGF21), a metabolic regulator on obese patients with type 2 DM. The study found favorable improvements in blood glucose levels, fasting insulin, body weight and adiponectin [ 114 ].

A 54-week randomized phase 2b study on Cotadutide, a GLP-1 and glucagon receptor agonist, demonstrated a significant decrease in HbA1c levels, body weight, and improvements in lipid profile and liver function tests at weeks 14 and 54 [ 115 ]. In a cross-sectional study conducted on Japanese adults, the administration of Blautia wexlerae , a commensal bacterium, demonstrated an inverse relationship with obesity and type 2 DM [ 116 ].

Dapagliflozin, canagliflozin and empagliflozin act by inhibiting sodium-glucose co-transporter 2 (SGLT2) in the kidney, blocking glucose reabsorption in the proximal tubule. More recent studies have reported that these drugs are effective in decreasing HbA1c levels and weight loss [ 117 ].

6. Management

Weight loss is the most efficient strategy for reducing the complications and comorbidities of type 2 DM. A moderate weight loss of 5 to 10% is sufficient to achieve normal blood pressure, glycemic control and increased HDL cholesterol levels [ 118 ]. Gradual weight loss leads to a decrease in adipocyte size, which in turn downregulates pathways involved in lipogenesis and oxidative stress [ 118 ]. Exercise is a key component of lifestyle interventions to achieve healthy weights and improve blood glucose levels, insulin sensitivity and lipid profiles. Most scientific guidelines recommend at least 150 min per week of moderate aerobic exercise combined with three weekly sessions of muscle strength resistance exercises. While exercise is crucial for weight loss, a combined approach of exercise and an energy-restricted diet such as a low-fat, low-carbohydrate and high-protein diet delivers better results [ 119 ]. The essential pillars in managing obesity and type 2 DM are dietary modifications and lifestyle interventions, although these can be challenging to maintain over time. Recently, different drugs have been approved to improve type 2 DM and promote weight loss such as GLP-1 receptor agonists and SGLT2 inhibitors [ 4 ].

Given the association between obesity and type 2 DM, a suitable anti-diabetic treatment for obese patients with diabetes should focus on preventing further weight gain while also using glucose-lowering agents that support weight reduction such as metformin therapy [ 120 ].

In the United States, a commonly used combination for type 2 DM and obesity management is Liraglutide with naltrexone and bupropion [ 121 ]. Metformin is the most prescribed FDA-approved medication for lowering blood sugar levels, as it increases insulin sensitivity and reduces glucose production in the liver. It also promotes weight loss and decreases food intake [ 122 ].

Bariatric surgery is highly beneficial for patients who are morbidly obese with a BMI of40 kg/m 2 or higher or for patients with type 2 DM and a BMI of 35 kg/m 2 or higher. This surgery effectively reduces cardiovascular events associated with morbid obesity and type 2 DM [ 123 ].

Other areas of therapeutic interest include “prebiotics”, which have been shown to improve glucose tolerance. This was demonstrated in mice on a high-fat diet that were fed prebiotics [ 124 ]. Another approach is the use of “probiotics”, which are enriched with live bacterial strains such as Bifidobacteria and Lactobacilli . These alter the gut microbiota and have been proven to be beneficial in type 2 DM by improving lipid profiles and reducing endotoxemia [ 125 ]. Several studies have reported a lower prevalence of type 2 DM and a healthy BMI in populations that consume significant amounts of polyunsaturated fatty acids, primarily found in fish [ 126 ].

Recently, intermittent fasting has been proven to be beneficial for weight reduction and improving glucose tolerance. It does this by selectively stimulating the activation of beige adipocytes in white adipose tissue (WAT) to promote “WAT browning” and by regulating the composition of intestinal microbial products, such as acetate and lactate which are known inducers of WAT browning [ 127 ].

• Obesity is a significant and modifiable risk factor associated with the development and progression of type 2 DM, and the increase in obesity is the primary factor in the recent rise in the prevalence and incidence of type 2 DM.
• It is crucial to understand the role of obesity in the pathogenesis of type 2 DM, considering the various factors and complications associated with the condition.
• Obesity is a chronic progressive condition characterized by excessive and abnormal fat accumulation in the body, resulting from the consumption of more calories than the body can use, with a Body Mass Index ≥ 30 kg/m 2 .
• Type 2 DM is a chronic metabolic condition characterized by insulin resistance where the body is unable to effectively use insulin, leading to high blood glucose levels or hyperglycemia.
• Currently, over half a billion people worldwide have been diagnosed with diabetes, and this number is projected to more than double to 1.3 billion in the next 30 years.
• According to the World Obesity Federation 2023 atlas, it is predicted that over 51% of the global population will become overweight or obese in the next 12 years.
• Obesity and type 2 DM are intertwined in their pathophysiology and molecular mechanisms, influenced by various factors such as adipose tissue, homeostatic factors like adiponectin, body fat distribution, inflammation, free fatty acids, gut microbiome and dyslipidemia. Therefore, it is crucial to understand this close relationship in order to effectively manage and prevent these conditions as an urgent response to their alarming global rise.
• Numerous in vivo and clinical studies have highlighted the significance of a comprehensive management approach that addressed both obesity and type 2 DM simultaneously. This approach is essential for effectively handling these chronic and interconnected conditions.

8. Conclusions

The prevalence rates of obesity (BMI ≥ 30 kg/m 2 ), extreme obesity (BMI ≥ 40 kg/m 2 ) and central obesity are rising worldwide. This trend is likely to contribute to the global epidemic of type 2 DM in the coming years. Obesity is strongly believed to promote type 2 DM, with adipose tissue, liver dysfunction and skeletal muscle dysfunction playing a central role. This connection has been suggested and demonstrated by numerous significant in vivo and clinical studies. Gaining a better understanding of the relationship and causality between these factors could provide an opportunity to predict, modify and monitor the risk, as there is substantial evidence that weight loss interventions can reduce blood glucose levels. There is an urgent need for the discovery and development of multi-targeted compounds that can treat both of these conditions. Therefore, a promising opportunity for drug discovery lies in comprehensive and deeper understanding of the mechanistic links between these closely intertwined conditions.

Acknowledgments

The authors are grateful to Sabine Weiskirchen (IFMPEGKC, RWTH University Hospital Aachen, Germany) for helping in drawing Figure 3 , Figure 4 , Figure 5 and Figure 6 for this review.

Abbreviations

Funding Statement

R.W. is supported by the German Research Foundation (grants WE2554/13-1, WE2554/15-1, and WE 2554/17-1), the Deutsche Krebshilfe (grant 70115581) and the Interdisciplinary Centre for Clinical Research within the faculty of Medicine at the RWTH Aachen University (grant PTD 1-5). The funders had no role in the design of this article or in the decision to publish it.

Author Contributions

Conceptualization, P.C.; resources, R.W.; data curation, P.C. and R.W.; writing—original draft preparation, P.C.; writing—review and editing, P.C. and R.W.; supervision, R.W.; funding acquisition, R.W. All authors have read and agreed to the published version of the manuscript.

Institutional Review Board Statement

Not applicable.

Informed Consent Statement

Data availability statement, conflicts of interest.

The authors declare no conflicts of interest.

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