Evaluation of the hepatic expression of microRNAs related to lipid metabolism in the offspring of mice with diet-induced obesity

Abstract

Obesity has acquired characteristics of an epidemic and the most recent figures indicate an expressive increase the prevalence of obesity among young people. The same figures indicating the increase in obesity also show a significant increase of individuals with diabetes type II. It is known that both pathologies are a metabolic response feature, which leads to a change in the synthesis of lipids and glucose homeostasis. The use of high-fat diet is responsible for fat mass increase, through the formation and maturation of adipocytes, predisposes to a greater deposit of triglycerides liver and activates the expression of microRNAs related to metabolic effects observed. Although studies demonstrate the effects of the use of high-fat diet during gestation, few studies have sought understand how the damage is starting in the cell. We believe that the offspring of mothers obese presents modulation in gene expression that can activate the synthesis of lipids (fatty acids and cholesterol), as well as inhibit the oxidation of lipids, resulting in the development of a "metabolic phenotype" amended, or simply "imprint metabolic", characteristic of increase in fat deposit in the liver, fat mass increase and the imbalance between the expense and energy consumption. To test this hypothesis will be assessed serum biochemical parameters, the activation of proteins in the liver indicating mainly changes in lipid metabolism and the expression of microRNAs liver that participate in the metabolic control of body.