Abstract

The increment in energy-dense food and low physical activity has contributed to the current obesity pandemic, which is more prevalent in women than in men. Insulin is an anabolic hormone that regulates the metabolism of lipids, carbohydrates, and proteins in adipose tissue, liver, and skeletal muscle. During obesity, nutrient storage capacity is dysregulated due to a reduced insulin action on its target organs, producing insulin resistance, an early marker of metabolic dysfunction. Insulin resistance in adipose tissue is central in metabolic diseases due to the critical role that this tissue plays in energy homeostasis. We focused on sexual dimorphism on the molecular mechanisms of insulin actions and their relationship with the physiology and pathophysiology of adipose tissue. Until recently, most of the physiological and pharmacological studies were done in males without considering sexual dimorphism, which is relevant. There is ample clinical and epidemiological evidence of its contribution to the establishment and progression of metabolic diseases. Sexual dimorphism is a critical and often overlooked factor that should be considered in design of sex-targeted therapeutic strategies and public health policies to address obesity and diabetes.

Highlights

  • One of the complex problems in modern society is that the availability of energy-dense food has led to an imbalance between the calories consumed and burned

  • This work aims to analyze the sex-specific mechanisms of the regulation of adipose tissue function by insulin to gain a better insight into the molecular mechanisms associated with developing metabolic diseases

  • The HSL lipolytic enzyme activity is blunted in adipose tissue of female Irs-2 -/- mice and this decreases the adverse effects of circulating lipids in females. These results suggest that IRS2 may play a sexually dimorphic role in the regulating insulin sensitivity in adipose tissue function [103]

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Summary

Introduction

One of the complex problems in modern society is that the availability of energy-dense food has led to an imbalance between the calories consumed and burned. A sedentary lifestyle has induced this imbalance. These factors undoubtedly have contributed to the recent obesity and diabetes pandemic and the increase in cardiovascular diseases. Epidemiological data reveal differences in the incidence and prevalence among men and women of overweight, obesity, metabolic syndrome, and as a consequence, type-2 diabetes mellitus (T2DM) and cardiovascular diseases (CVDs). Clinical and experimental evidence of sex-specific components in the development of these diseases supports these facts [2]. The genetics and molecular mechanisms underlying these different responses are not entirely clear

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