Abstract

Obesity is a major risk factor for the development of insulin resistance and type 2 diabetes. The exact mechanism by which adipose tissue induces insulin resistance is still unclear. It has been demonstrated that obesity is associated with the adipocyte dysfunction, macrophage infiltration, and low-grade inflammation, which probably contributes to the induction of insulin resistance. Adipose tissue synthesizes and secretes numerous bioactive molecules, namely adipokines and cytokines, which affect the metabolism of both lipids and glucose. Disorders in the synthesis of adipokines and cytokines that occur in obesity lead to changes in lipid and carbohydrates metabolism and, as a consequence, may lead to insulin resistance and type 2 diabetes. Obesity is also associated with the accumulation of lipids. A special group of lipids that are able to regulate the activity of intracellular enzymes are biologically active lipids: long-chain acyl-CoAs, ceramides, and diacylglycerols. According to the latest data, the accumulation of these lipids in adipocytes is probably related to the development of insulin resistance. Recent studies indicate that the accumulation of biologically active lipids in adipose tissue may regulate the synthesis/secretion of adipokines and proinflammatory cytokines. Although studies have revealed that inflammation caused by excessive fat accumulation and abnormalities in lipid metabolism can contribute to the development of obesity-related insulin resistance, further research is needed to determine the exact mechanism by which obesity-related insulin resistance is induced.

Highlights

  • Epidemiological studies on obesity and overweight demonstrate that these are significant, constantly growing problems that have reached the status of global epidemics

  • An increase in the supply of energy substrates in relation to the body’s requirements leads to the accumulation of their excess in adipose cells in lipogenesis process. This process is regulated by insulin, which increases the activity of lipoprotein lipase (LPL) stimulating the hydrolysis of TAGs circulating in plasma in combination with albumins, chylomicrons or very low-density lipoproteins (VLDL), allowing free fatty acids (FFA) to enter the cell

  • Obesity is defined as an excessive accumulation of adipose tissue in the body, which contributes to overall health impairment

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Summary

Introduction

Epidemiological studies on obesity and overweight demonstrate that these are significant, constantly growing problems that have reached the status of global epidemics. There are a number of causes leading to the development of obesity, including genetic and environmental factors. Insulin, secreted by β cells located in pancreatic islets, is an anabolic hormone that causes glycogen accumulation in the liver and skeletal muscles This hormone lowers blood glucose levels by increasing glucose uptake by muscles and adipose tissue, stimulates glucose oxidation and glycogenesis, and inhibits gluconeogenesis and glycogenolysis. It stimulates lipogenesis and inhibits lipolysis, which leads to the storage of free fatty acids (FFA) in the form of triacylglycerols (TAG) in adipose tissue. Insulin has a wide spectrum of effects on metabolic processes in adipocytes; it is considered the most important hormone regulating anti-lipolytic processes, and deterioration of cell sensitivity to this hormone or impairment of the insulin pathway may affect the metabolism of adipose tissue

Type of Obesity Adipose Tissue Localization and Insulin Resistance
Lipid Metabolism in Adipose Tissue
Biologically Active Lipids
Adiponectin
Leptin
Apelin
Resistin
Summary
Findings
Overview

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