Body mass index has a strong relationship to diabetes and insulin resistance. In obese individuals, the amount of nonesterified fatty acids, glycerol, hormones, cytokines, proinflammatory markers, and other substances that are involved in the development of insulin resistance, is increased. The development of diabetes becomes more inevitable if the failure of β-islet cells of the pancreas is accompanied by insulin resistance. Weight gain and body mass are central to the formation and rising incidence of type 1 and type 2 diabetes.
Overweight and obesity are defined by an excess accumulation of adipose tissue to an extent that impairs both physical and psychosocial health and well-being. Obesity is considered a health disaster in both developed and developing countries.
The prevalence is escalating significantly in many nations worldwide. This pandemic needs to be stopped if the economic costs, social hazards, morbidity, and mortality of the disease are considered.
Obesity and type 1 diabetes
The rising incidence of type 2 diabetes among children and adults is related to the epidemic of obesity. A similar etiology is also responsible for a similar increase in type 1 diabetes. While the underling pathophysiology of type 1 diabetes, which is autoimmune in nature, continues to be investigated and studied, the exact mechanism causing the rise in the incidence of type 1 diabetes remains unclear, particularly in young age groups. The etiology of type 1 diabetes, according to twin studies, indicates a joint contribution of environmental and genetic factors. Furthermore, the importance of environmental factors in the etiology of diabetes is indicated by a significant rise in type 1 diabetes incidence in immigrants from lower to higher incidence regions. Multiple triggers for the development of type 1 diabetes have been investigated, including short- duration or the absence of breastfeeding, exposure to cow’s milk protein, and exposure to some kind of infection such as enterovirus or rubella. However, none of these triggering factors has been shown to be the definitive cause.
Obesity and type 2 diabetes
The increased prevalence of obesity these days has drawn attention to the worldwide significance of this problem.
Both type 2 diabetes and obesity are associated with insulin resistance. Most obese individuals, despite being insulin resistant, do not develop hyperglycemia. Pancreatic β-cells of the islet of Langerhans release adequate amounts of insulin that are sufficient to overcome insulin level reductions under normal circumstances, thus maintaining normal glucose tolerance.
Throughout the natural history of type 2 diabetes, endothelial dysfunction is accompanied with obesity/insulin resistance in diabetes and prediabetes conditions (this includes people with impaired glucose tolerance and/or impaired fasting glucose). In order to develop insulin resistance and obesity, thereby causing type 2 diabetes, β-cells should not be able to compensate fully for decreased insulin sensitivity. The nonesterified fatty acids (NEFAs) that are secreted from adipose tissue in obese people may lead to the hypothesis that insulin resistance and β-cell dysfunction are most likely linked.
Obesity and insulin resistance
Insulin sensitivity fluctuation occurs across the natural life cycle. For example, insulin resistance is noticed during puberty, in pregnancy, and during the aging process. In addition, lifestyle variations, such as increased carbohydrate intake and increased physical activity, are associated with insulin sensitivity fluctuations. Obesity is considered the most important factor in the development of metabolic diseases. Adipose tissue affects metabolism by secreting hormones, glycerol, and other substances including leptin, cytokines, adiponectin, and proinflammatory substances, and by releasing NEFAs. In obese individuals, the secretion of these substances will be increased.
Insulin sensitivity is determined by another critical factor, which is body fat distribution. Insulin resistance is associated with body mass index at any degree of weight gain. Insulin sensitivity also differs completely in lean individuals because of differences in body fat distribution. Individuals whose fat distribution is more peripheral have more insulin sensitivity than do individuals whose fat distribution is more central (ie, in the abdomen and chest area).
Furthermore, abdominal fat is considered more lipolytic than subcutaneous fat, and it also does not respond easily to the antilipolytic action of insulin, which makes intra-abdominal fat more important in causing insulin resistance, and thus diabetes.
Obesity and β-cell dysfunction
β-cells play a vital role in regulating insulin release, despite their fragility. The quantity of insulin released by β-cells fluctuates and changes according to the quantity, nature, and route of administration of the stimulus. Therefore, β-cells play a very important role in ensuring that in healthy subjects, concentrations of blood glucose are stable within a relatively normal physiological range. In obesity, insulin sensitivity, as well as the modulation of β-cell function, decreases.
Diabetes and obesity are chronic disorders that are on the rise worldwide. Body mass index has a strong relationship to diabetes and insulin resistance. In an obese individual, the amount of glycerol, hormones, cytokines, proinflammatory substances, and other substances that are involved in the development of insulin resistance are increased. Insulin resistance with impairment of β-cell function leads to the development of diabetes. Gaining weight in early life is associated with the development of type 1 diabetes.