DIET-INDUCED ASPECTS OF AN EXPERIMENTAL MODEL OF OBESITY

Abstract

Obesity is currently one of the most widespread pathologies. In Uzbekistan, obesity and conditions associated with it affect 20.4% of the total population; specifically, this figure stands at 22.1% among women and 11.5% among men [3]. Diseases linked to metabolic syndrome—particularly obesity—drive an increase in the incidence of type 2 diabetes and prediabetes. The specific activity of visceral adipose tissue exacerbates insulin resistance, as this tissue is characterized by high lipolytic activity and a diminished response to the antilipolytic action of insulin. Consequently, levels of free fatty acids rise, and high concentrations of these acids enter the liver, inducing hyperglycemia, hyperinsulinemia, and insulin resistance; this, in turn, increases triglyceride synthesis and lowers levels of high-density lipoprotein (HDL) cholesterol [1]. Adipose tissue—especially visceral fat— produces leptin, tumor necrosis factor (TNF), various growth factors, angiotensinogen, and a range of other hormonally active substances. The overproduction of these substances leads to a desensitization of the hypothalamus and the subsequent development of insulin resistance within the context of metabolic syndrome [2]. Debate persists regarding which of these factors plays the primary role in the pathogenesis of metabolic syndrome: insulin resistance, hyperinsulinemia, or obesity.