Diabetes mellitus (DM) is a chronic disease that is capable of changing the metabolism of protein, carbohydrate and fat. The disorder is a result of the unavailability of insulin secretion caused by the inability of the beta Langerhans islet cells found in the pancreas to secrete insulin, or it’s caused by the complications in the uptake of insulin in the proximal body tissues. DM is further categorised into two groups namely type 1 and type 2 diabetes (Kahn, Cooper, & Del Prato, 2014). Type 1 diabetes (T1D) is most prevalent in children, however it can sometimes occur in adults, especially those age thirty years and above. It is commonly the case that type 1 diabetic patients are not obese but are often diagnosed with diabetes ketoacidosis which is an emergency status (American Diabetes Association, 2014).
The pathophysiology of type 1 diabetes shows that it is an autoimmunity (Stankov, Benc, & Draskovic, 2013). The prevalence of type 1 diabetes is highest in the presence of other autoimmune diseases such as Addison’s disease. The pathophysiology and aetiology of type 2 diabetes (T2D) is rather different from type 1 diabetes. The prevalence of type 2 diabetes increases with the increasing presence of diabetes among other factors associated with it such as physical inactivity, unhealthy diet, and urbanization (Tai, Wong, & Wen, 2015).
The increasing cases of obesity in both adults and children have been associated with the corresponding rise in the incidence of type 2 diabetes (Bhupathiraju, & Hu, 2016). On the other hand, the specific mechanism which leads to the increased prevalence of type 1 diabetes is still under investigation. However, studies have shown that it is as a result of both environmental and genetic factors (Atkinson, Eisenbarth, & Michels, 2014). Other studies have also found out that there is a relationship between type 1 diabetes and weight gain (Baidal et al., 2016). There is a strong relationship between obesity and type 2 diabetes which are both related with insulin resistance. Type 2 diabetes is characteristic of endothelial dysfunction which has also been associated with insulin resistance or obesity. Weight gain and insulin resistance causes type 2 diabetes due to the inability of beta cells to fully compensate for the poor insulin sensitivity (Ye, 2013).
Diabetes and obesity have not only reached epidemic levels but have become public health issues in the United States and worldwide. Global statistics indicate that obesity is a much bigger problem than hunger, and the major cause of morbidity and death across the globe with this state of conditions expected to increase in the future. Almost one out of 10 adults in the US have diabetes with 90% of these being diagnosed with type 2 diabetes. It has historically been assumed that diabetes is an adult disorder, but the recent rise in body weight in children and young adults have led to the rise in the type 2 diabetes cases, more so among the Hispanic young adults (46.1%) and Blacks (57.8%) (Menke, Casagrande, Geiss, & Cowie, 2015). The management and treatment of obesity and diabetes is too costly (American Diabetes Association, 2013). The healthcare expenses for obese patients is higher by 42% compared to those of normal-weight, whereas it is double the rate for diabetic patients compared to non-diabetic individuals (Mozaffarian et al., 2015). Both diabetes and obesity are correlated, intricate disorders which can significantly be prevented and treated (Ley, Hamdy, Mohan, & Hu, 2014). Both diseases increases the risk for cardiovascular illnesses and cerebrovascular accident. Owing to the cost and increasing incidences of both diabetes and obesity cases across the globe, it is important that critical analysis is done on the studies that explore the association between the two conditions. This paper provides a critical review of modern literature on the links between obesity and diabetes.
Inclusion and Exclusion Criteria
The researcher critically investigated appropriate articles and books relevant to the study topic. Search engines like Google Scholar, PubMed, PMC, and BMC to carry out a systematic research to find out the studies that focused on diabetes and obesity. The search was only restricted to articles published within five years. The articles had to be on the link between diabetes and obesity. 80 studies were retrieved from the databases after identification, screening, and quality check. 50 articles were then included for assessment. 10 articles were not included due to duplication. Out of the 40 remaining articles, fifteen of them were being sold and thus did not have open access. Further suitability assessment led to the exclusion of ten more studies leaving the researcher with fifteen articles that fully met the inclusion criteria. Among the fifteen articles, eight of them were literature reviews and the other seven were primary articles. As a result of the critical review, different themes were ascertained such as theoretical models, research methodologies, and the synthesis of the findings as shown in the literature section of this paper.
The key search terms used during the research include obesity, diabetes mellitus, type 1 diabetes, type 2 diabetes, diabetes management, diabetes prevention, insulin resistance, and prevalence.
Theoretical Models
The researcher ascertained several theories which explain the relationship between diabetes and obesity or weight gain.
Accelerator Hypothesis
The study by Al-Goblan, Al-Alfi, and Khan (2014) examined the accelerator hypothesis and found a significant association between diabetes and obesity. The authors ascertained that the risk of developing type 1 diabetes was significantly associated with weight gain among youths. This is because the increase in body weight fosters insulin resistance, thus causing the development of type 1 diabetes in people who are genetically predisposed to diabetes. Similarly, type 2 diabetes and obesity are linked to insulin resistance because of the inability of the beta cells to fully compensate for the low insulin sensitivity. Obesity or insulin resistance in pre-diabetes or diabetic conditions are influenced by the endothelial dysfunction.
Excessive FFAs and Ectopic Fat-Storage Syndrome
Saboor Aftab, Reddy, Smith, and Barber (2014) theorised that overall and abdominal adiposity is closely related to the development of T2D, pointing out to the significance of waist diameter in clinical evaluation (Scott et al., 2014). Factors such as abdominal obesity, BMI measurement, and sagittal abdominal diameter are implications for the primary role of central adiposity in the development of T2D (Pajunen et al., 2013). High levels of visceral fat leads to excessive production of free fatty acids (FFAs) which end up reaching the liver through the portal vein causing fatty liver. This condition is linked to increased levels of non-esterified fatty acid (NEFA) in the plasma which consequently leads to insulin resistance through the Randle’s effect in the proximal body tissues such as muscles which are also the targets of insulin (Byrne, & Targher, 2014; Ye, 2013). In the hypothesis of ectopic fat storage, there seems to exist a depot limit for the visceral tissue, outside which the expanding depot of the adipose tissue cannot properly store the increased fat (Choe, Huh, Hwang, Kim, & Kim, 2016; Boren, Taskinen, Olofsson, & Levin, 2013). As a result, the excess fat is deposited in the sites of extra adipose tissue such as skeletal muscles, liver among others, leading to elevated levels of insulin resistance, damaged function of the beta cells and finally T2D (Lafontan, 2014; Rutkowski, Stern, & Scherer, 2015). Vasques et al. (2015) also found out that sagittal abdominal circumference could be used as a predictor of insulin resistance among people of different ethnicities.
The adipocytokines are also believed to be instrumental in the development of T2D that is associated with obesity. The obese adults undergo expansion of fat mass which causes the adipocytes to secret fatty acids, different adipocytokines and inflammation of mediators (McGown, Birerdinc, & Younossi, 2014; Blüher,2014). The adipose tissue then responds to the varying nutrient and neuro-hormonal indicators by producing adipocytokines that regulate eating, immunity, and thermogenesis. Consequently, the sensitivity of insulin towards the various organs of target are altered by the adipocytokines, and thus leading to obesity which is associated with T2D (Nakamura, Fuster, & Walsh, 2014; Smitka, & Marešová, 2015).
Gut Microbiota and the Development of Obesity and Type 2 Diabetes
There is evidence of a strong relationship between gut microbiota and the development of obesity by influencing different factors such as increasing food intake, intestinal permeability, and inflammation among others (Devaraj, Hemarajata, & Versalovic, 2013; Naseer et al., 2014). This theory is based on the findings that some types of bacteria belonging to the gut microbiota are actively responsible for the uptake of nutrients and dispensing energy. Whereas the lipopolysaccharide (LPS) which is secreted in the gut which is home to several microbes may be an inducing element and linking inflammation to the unhealthy diet characteristic of excess fats which causes obesity (Devaraj, Hemarajata, & Versalovic, 2013). The gut microorganisms increase the absorption of monosaccharide from the intestinal tract and trigger the host to increase the hepatic secretion of triglycerides. This activity fosters elevated levels of insulin resistance (Mikkelsen et al., 2015).
Severe Inflammation and the Activation of the Immune System
Esser, Legrand-Poels, Piette, Scheen, and Paquot (2014) theorised that severe inflammation and the activation of the immune system triggers insulin resistance which is associated to both T2D and obesity. The common sites of inflammation in obese cases include the muscles, liver, and adipose tissue. The permeation of some immune cells and macrophages takes place in these organs causing a shift in cell population which enhances inflammation. These cells are vital in the secretion of cytokines which encourage inflammation and thus altering the signalling of insulin in the proximal tissues or trigger the dysfunction of beta cells leading to inadequate insulin.
Obesity which leads to type 1 diabetes is as a result of lack of physical activity. Being physically active increases fitness in people with T1D, however the decreased fitness level in youths is an indication of low aerobic power and strength. The routine involvement in physical activities is enhances lipid levels, insulin resistance, and endothelial function, with the exception of blood pressure in people with type 1 diabetes (Minges, Whittemore, & Grey, 2013; Liese, Ma, Maahs, & Trilk, 2013).
Occupational Risk and Lifestyle Factors
Poulsen, Cleal, Clausen, and Andersen (2014) found out that both occupational risk and lifestyle factors were influential in developing diabetes. BMI above the normal body weight is the most significant risk factor. Furthermore, overweight is related with physical inactivity, shift work, and issues to do with sleep and health. According to Ganz, Wintfeld, Li, Alas, Langer and Hammer (2014) there is a strong independent association between BMI and the risk of developing T2D. The higher the BMI the higher the chances of being diagnosed with T2D. Metabolic syndrome is high among employees due to their nature of lifestyle which is sedentary. This can be attributed to the socioeconomic changes and transitions in diet among employees. Overweight is the leading metabolic syndrome among employees of North East China in both genders (Wang et al., 2015). Pulgaron and Delamater (2014) studied obesity and diabetes in children and demonstrates that factors such as individual history of obesity, culture, environment and genetic are attributed to obesity risk. Costa et al. (2016) also found out that the prevalence of obese cases in T1D children was highly associated with lifestyle behavioural factors such as consumption of unhealthy foods, low socioeconomic activities, and overfeeding from parents due to fear of hypoglycaemia. Bhupathiraju and Hu (2016) opined that abdominal obesity, changes in agricultural policies, trends in physical activity and napping, dietary changes, and genetics are the factors that foster obesity and diabetes.
Al-Goblan et al. (2014) conducted a literature review on the association between obesity and insulin resistance (diabetes mellitus). A review was similarly conducted by Saboor Aftab et al. (2014) on the complex relation between obesity and type 2 diabetes. Reviews on the function of the Gut microbiota in diabetes and obesity were conducted by Naseer et al. (2014) and Devaraj et al. (2013). Another literature review was conducted on the association between inflammation and obesity, T2D, and metabolic syndrome by Esser et al. (2013). Minges et al. (2013) used a systematic literature review to assess the link between physical activity, nutrition, sleep, and sedentary lifestyle and obesity in young adults diagnosed with type 1 diabetes. A literature review was also conducted by Pulgaron and Delamater (2014) on obesity and T2D in children.
Vasques et al. (2015) used a multicentre population survey to ascertain whether sagittal abdominal diameter could be used as a predictor of insulin resistance. Poulsen et al. (2014) conducted a prospective cohort study using questionnaire to explore the relationship between job, obesity and diabetes. A case control study was used by Ganz et al. (2014) to ascertain the link between body mass index and the risk of being diagnosed with T2D. Wang et al. (2015) carried out a health screening of employees in North East China to approximate the metabolic syndrome (overweight, T2D) prevalence among them. An analytical cross-sectional study was conducted on type 1 diabetes to determine the frequency of obese cases in children diagnosed with T1D and the associated factors (Costa et al., 2016). A cohort follow-up study was conducted on healthy young adults to ascertain the incidence of diabetes overtime (Twig et al., 2014). Lukács, Kiss-Tóth, Csordás, Sasvári, and Barkai (2018) conducted a population based quantitative study to assess the associated risks of T2D in adolescent students diagnosed with overweight and obesity.
A literature review on the association between obesity and insulin resistance was conducted by Al-Goblan et al. (2014). The authors found out that there was a significant association between BMI and diabetes and insulin resistance. The findings indicate that there is an increase in the quantities of glycerol hormones, NEFA, among other substances that are active in the development of insulin resistance in obese people. Furthermore, the impairment of the function of beta cells alongside insulin resistance causes diabetes development. Excessive weight at an early age is related to development of T1D. The authors also found out that NEFA was key in the initiation of insulin resistance and in the compromise of the functionality of beta cell.
Saboor Aftab et al. (2014) carried out a literature review on obesity and T2D and found out that diabesity is as a result of the continued and excessive intake of energy-dense foods and physical inactivity. Excessive intake of energy-dense foods caused increased fat deposition and fosters insulin resistance. A fatty liver is caused by the release of free fatty acids (FFA) to the liver through the portal vein. The spill of FFA into the systemic circulation leads to liptoxicity of body tissues such as the heart and muscles causing a viscid cycle of fat damage and inflammation which worsens insulin resistance, dysfunction of beta cells and finally the development of type 2 diabetes. Furthermore, the authors ascertained that an independent determinant of insulin resistance is visceral fat content whereas adipokines prevent the development of type 2 diabetes which is caused by obesity.
Naseer et al. (2014) conducted a literature review and examined the function of gut microbiota in T2D, obesity and Alzheimer’s disease and showed that there was a relationship between the human microbial flora and the manifestation of metabolic syndrome such as T2D, obesity and other related illnesses. The gut microbiota regulates energy balance and adiposity in the host through different process such as the rise in the uptake of energy from nutrition, regulation of the composition of tissiue fatty acid, the modulation of peptides secreted in the gut and bile acids. The microbiota gut is also influential in the metabolism of sugar and lipid and in the LPS development which both fosters low grade inflammation in obesity and type 2 diabetes which is obesity-based. Similar studies were conducted by Deveraj et al. (2013) and found out that the gut microbes had a substantial positive effect on the metabolic syndrome, diabetes and obesity. Elevated levels of FFA and hyperglycemia are the typical features of obesity, diabetes, and metabolic syndrome, alongside a diet with excess fat and energy dense foods. All these increasingly activates the inflamasome complex in addition to increasing the activation of macrophages. Moreover, macrophages can penetrate the adipose tissue and trigger mitogen-triggered protein kinases leading to elevated cross-talk and adipokines. A diet rich in fat and hyperlgycemic one causes alterations in the gut microbiome by changing the content of histidine among others causing dysfunction of the gut and conditions common in diabetes, obesity and metabolic syndrome by altering the response of the host.
Likewise, Esser et al. (2014) conducted a review on the association of inflammation between T2D, obesity and metabolic syndrome and showed that low-grade inflammation and a triggered immune system had a central role in the development of insulin resistance associated to obesity and T2D. Vasques et al. (2015) carried out a survey on a women population of multiple races to determine whether sagittal abdominal diameter (SAD) can be used as a predictor of insulin resistance (IR). The findings indicate that there was a substantive positive correlation between the adjusted age and total body fat mass and the BMI with the measured IR. The women with high sagittal abdominal diameter were three times more likely to be diagnosed with insulin resistance compares with those with normal sagittal abdominal diameter. On the other hand, the participants with increased BMI and waist circumference were twice more likely to have insulin resistance. The study was of clinical relevance as it was the first to examine the use of SAD in the screening of insulin resistance in an ethnically diverse population of adult women. However, the study did not validate SAD as a predictor of clinical outcomes in the population of Brazil.
Minges et al. (2013) carried a systematic review to assess overweight and obesity in youth diagnosed with T1D with a particular focus on their association with physical activity, napping, nutrition, and sedentary lifestyle. The authors found out that overweight in T1D youths was related to irregular sleep, too much TV watching, and skipping dinner and breakfast, however, there was no association with physical activity. Wight management mechanisms showed progressive weight loss alongside better glycemic control. The study points out the existing gap in the literature on the previous studies and impacts of too much weight gain in children diagnosed with T1D, thus prompting further research.
Poulsen et al. (2014) carried out a prospective cohort study on healthcare workers to ascertain the association between work, obesity and diabetes. The results show that 3.5% of the respondents had manifestations of diabetes which was linked to obesity, overweight and age. Obesity was much prevalent in the young workers and was strongly related with the manifestation of diabetes and physical inactivity. The study confirmed that the most influential risk factor for diabetes was obesity which was also determined by some occupational risk factors. However, the baseline measures in this study were only based on self-report thus raising the issue of reliability, but the large sample size in addition to the high response rate increases the generalizability of the findings.
Ganz et al. (2014) carried out a case-control study using the electronic health database in the US to ascertain the link between BMI and the risk of T2D.The outcomes showed a significant positive independent association between BMI and the risk of developing type 2 diabetes. However, the study did not assess the causal impact of BMI on the risk of developing type 2 diabetes due to the utilization of a retrospective cohort approach. Furthermore, the analysis was only based on one integrated health system meant for Pennsylvania population thus limiting generalizability to extensive population and in different settings.
A study on the prevalence of metabolic syndrome among North East China employees was carried out by Wang et al. (2015). The metabolic syndrome definitions consisted of abdominal obesity, elevated glucose fasting among others. The results indicated high prevalence of metabolic syndrome with overweight being the most common in men (54.7%) and women with central obesity accounting for 35.9% both of which are risk factors in the development of diabetes. The study of Wang and colleagues is based on a large sample size of workers in china and is the first study to scientifically investigate the incidence of metabolic syndrome among workers of china. However, the study might have underestimated the incidence of metabolic syndrome among the workers in Northeast China due to the absence of information.
Pulgaron and Delamater (2014) in their literature review on the epidemiology and management of T2D and obesity ascertained several factors that lead to the two disorders. The authors found out that overweight in children increases the possibility of being diagnosed with obesity in the later years. The prevalence of T2D is much higher in youths with a family background of type 2 diabetes and obesity. Additionally, incidences of obesity and T2D are lower in youths from lower income families and ethnic minority. Costa et al. (2016) also assessed overweight in young adults and children diagnosed with T1D with an emphasis on the incidence and related factors. The study found out that there was a high incidence of overweight among the children and adolescents with T1D. This was majorly attributed to unhealthy eating habits and sedentary lifestyle. These findings were supported by previous studies (Meissner et al., 2014). Twig et al. (2014) also found out that the prevalence of diabetes was linked to obesity and overweight, and the absence of diabetes risk factors and presence of health metabolic profile were not an a safeguard against diabetes. The study was however focused on men only thus restricting its replication in a population of women. The quantitative study undertaken by Lukács et al. (2018) on the factors for T2D in obese and overweight students in school indicates that the young adults are more prone to diabetes and overweight. This study was however limited in that the screening of risk factors for the manifestations of T2D was only done on the obese and overweight students, and yet the disorder can take place in individuals with normal body mass.
The outcomes of the review show a strong positive significant link between obesity and diabetes. Weight gain or diabetes is associated to diabetes by fostering insulin resistance and the dysfunction of beta cells. The fluctuation in insulin sensitivity takes place in different stages of life such as during pregnancy and in the process of aging. Furthermore, lifestyle behaviours such as sleep, physical activity and elevated intake of carbohydrates also affect the variations in insulin sensitivity. However, studies have indicated that obesity is the most common factor that influences the manifestation of metabolic diseases. The body metabolism is affected by the adipose tissue through hormonal secretion such as cytokines and the secretion of NEFAs. The rate of secretion of these substances is much higher in obese people. Insulin insensitivity is majorly impacted by the secretion of the NEFAs. Both T2D and obesity are characteristic of elevated production levels of NEFAs which is also linked to insulin resistance in both cases. Fat distribution is another factor which is also a determinant of insulin sensitivity. BMI at any level of weight gain is linked to insulin resistance. In other words, people with increased peripheral fat distribution have higher levels of insulin sensitivity compared to those with centralised fat distribution especially in the abdomen and chest. The dysfunction of beta cells is also associated with diabetes. Beta cells are significant in moderating the release of insulin and the amount released is dependent on the nature, amount and path of stimulus administration. Thus, the beta cells make sure that the concentrations of blood sugar in health people is stabilised. The failure of the normal communication between insulin sensitive tissues and the beta cells causes instability in glucose levels and the development of diabetes. Excessive FFAs and ectopic fat storage are also associated to the development of T2D. Recent studies have also associated gut microbiota with the development of obesity and T2D. Severe inflammation and the activation of the immune system triggers insulin resistance which is associated to both T2D and obesity.
Limitations
As is always inherent with literature reviews, a number of limitations are prevalent. As much as this study exhaustively conducted a review of current studies relevant to the study topic, it is likely that some studies were not included in the analysis due to selection bias or publication. Nonetheless, the findings of this review can be moderated because the researcher did not find any extra manuscript from the searched list of reference.
Strengths
The review investigated current literatures of five years only. This implies that the findings are relevant to the current trend of the diseases and thus will provide vital information to both researchers and policy makers. The review included both reviews and primary data at the ratio of 8:7 respectively. This is strength to the study because the findings are based on analysis of both primary and secondary data thus increasing its credibility and findings. The review also followed an inclusion and exclusion criteria in the selection of articles for inclusion thus minimizing any possible selection bias. Furthermore, it ensured that only the relevant articles are included in the analysis, thus increasing the reliability and validity of the study. The review was not limited to any geographical setting thus increasing the possibility of generalizing the outcomes in any population setting.
Policy Implications
The findings of the review have policy implications on various aspects of healthcare services. The outcomes of the review can be a guide in policy planning and implementation in the department of health, schools and communities due to the evidence on the association between diet and diabetes and obesity or weight gain. Additionally, the study outcomes can be used designing policies on dietary guidelines for populations, schools or hospitals that have high risk of developing cardiovascular conditions
The department of health can also utilize the outcomes of the study to update its polices on the provision of healthcare services to individuals diagnosed with cardiovascular diseases based on the current trend in order to offer patient centred services
Key Stakeholders
Some of the key stakeholders to the findings of this study include the school administrations especially in the urban schools which have been shown to be at risk of developing obesity and diabetes. The school administration are key stakeholders because of the overwhelming evidence of the increasing cases of diabetes and obesity in school-age youths and children. They will find this information important in designing effective interventions
The department to health is also a potential stakeholder because its mission is to offer quality and effective healthcare services to the citizens. This study will be of essence to the department in designing and planning community based intervention programs aimed at preventing and managing the increasing prevalence of diabetes and obesity.
The hospital administrations are some of the potential stakeholders because of the increasing evidence of the effectiveness of behaviour approaches towards the prevention and management of diabetes and obesity, which is partially addressed in this review. Thus, the healthcare providers can be trained to integrate such approaches to the normal pharmacological approach.
Recommendations for Future Research
Further studies should be conducted on how to manage and prevent diabetes and obesity based on findings of this study. This is essential as this study considers the epidemiology and pathophysiology of the disorders, thus necessitating an intervention that works from cause to effect. There is need for researchers to focus on providing detailed information on the mechanisms in which varying bacterial groups in the gut can impact body metabolisms.
Conclusion
Obesity and diabetes are some of the most prevalent illnesses that are on the increase across the globe. This is despite of the numeral studies that have been done on the possible effective intervention to prevent and manage the disorders. The current trend shows that both type 1 and type 2 diabetes are prevalent in both children and adults, with noticeable high incidence among school going children and youths. This overwhelming increase in the incidences of the disease have attracted the attention of several researches aimed at ascertaining the association between obesity and diabetes and the corresponding risk factors. As a result, several theoretical models have been developed on the possible association between diabetes and obesity. These include Excessive FFAs and Ectopic fat-storage syndrome, the accelerator hypothesis, Gut microbiota and the development of obesity and type 2 diabetes, severe inflammation and the activation of the immune system, and occupational risk and lifestyle factors. The findings indicate that obese cases are much more prevalent in individuals with diabetes, and that obesity, BMI or weight gain plays a significant role in insulin resistance. There is an increase in the quantity of NEFA, hormones, and pro-inflammatory compounds in those with obesity because these substances are responsible for insulin resistance. A dysfunctional beta cell and insulin resistance results in the manifestation of diabetes.
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