Central obesity and insulin resistance, type 2 diabetes have significantly increased (P < 0.05). As shown in Table 3 for each group, the incidence of IGT (impaired glucose tolerance) and DM (diabetes mellitus), as well as IR (insulin resistance) after injection: Group B and Group C showed a significant difference compared to the control group (P < 0.054).
Obesity, especially central-type (abdominal) obesity, is closely related to pancreatic islet function, insulin resistance, and cardiovascular disease, representing an important pathogenesis of diabetes. Epidemiological data indicate that the prevalence of obesity in individuals with type 2 diabetes is significantly higher than in the general population [14]. Studies also reveal that the prevalence of diabetes increases significantly with obesity, reaching over 10%. In particular, the prevalence rates are centered around IGT (46.7%), DM (61.4%), and insulin resistance (83.9%) when compared to non-obese individuals, showing highly significant differences. Central obesity exhibits more significant differences than peripheral obesity in terms of BMI, waist-to-hip ratio (WHR), and IR, which are negatively correlated with IGT but positively correlated with the prevalence of DM. These findings align with relevant literature reports.
The description of abnormal body fat distribution indicates that excess fat storage in the abdomen compared to peripheral tissues poses a greater risk. The etiology of obesity is very complex and may be related to sex hormone secretion, increased androgen activity leading to abdominal fat accumulation, forming a central-type fat distribution. This could be due to the promotion of intra-abdominal preadipocytes into fat cells, increasing intra-abdominal fat cell counts. Female hormones promote peripheral fat deposition, while WHR is negatively correlated with plasma sex hormone-binding globulin (SHBG) levels and positively correlated with free testosterone levels. Increased glucocorticoid levels play a more significant role in the formation of central fat distribution compared to peripheral obesity. Scholars have found that women with central obesity exhibit increased urinary 17-hydroxysteroids and 17-ketosteroids, stimulated by ACTH, cortisol, aldosterone, and cortisol, which can promote insulin resistance. Additionally, genetics, eating habits, exercise, and other factors are related to obesity and insulin resistance in type 2 diabetes. At the molecular level, data show that obesity is often associated with fasting hyperinsulinemia or postprandial (or glucose) hyperinsulinemic responses. On the one hand, despite obesity and hyperinsulinemia, hypoglycemia is not easily induced or occurs minimally. Furthermore, when exogenous insulin is applied, the decline in glucose levels is smaller than normal. These indicate the presence of insulin resistance-induced hyperinsulinemia in obesity. There are two reasons for this: First, β-cell hypersecretion and reduced hepatic insulin clearance in obesity, where its clearance rate is negatively correlated with BMI and WHR. Obesity-induced insulin resistance is mainly due to reduced insulin receptor numbers, insulin receptor tyrosine activation abnormalities, second messenger abnormalities, and abnormal glucose transporters, contributing to insulin resistance. Body fat content and fat distribution type are two independent risk factors for central obesity, insulin resistance, and impaired glucose tolerance, with higher morbidity rates in diabetic patients. Free fatty acid release from fat cells in central obesity patients, compared to peripheral obesity, increases fasting plasma glucose levels and free fatty acid concentrations in the blood, enhancing muscle oxidation of fatty acids and reducing glucose entry into cells. It has been confirmed that increased free fatty acids in the human body induce peripheral tissue insulin resistance. This is one of the reasons why central obesity patients are prone to insulin resistance and diabetes.
In summary, central obesity is an important risk factor for insulin resistance and diabetes. Therefore, raising awareness of obesity and type 2 diabetes, understanding their mechanisms, and prevention have become critical health issues in today’s society.