Effect of High‐Sucrose and High‐Fructose Diets on Adipose Tissue Dysfunction and Metabolic Syndrome

Abstract

Metabolic Syndrome (MS) increases the risk of developing type 2 diabetes and cardiovascular diseases. Fructose is a key component shown to be associated with MS development in humans and animal models. High sucrose (HSD)‐ and high fructose‐diet (HFD)‐induced MS is well studied in animal models. In this study, for the first time we compared the effects of HSD and HFD on development of MS parameters including visceral obesity, dyslipidemia and insulin resistance.Weaning, male Wister rats were fed with diets containing starch, sucrose and fructose (60% w/w) for twelve weeks and tissues were collected for analysis. Plasma glucose, insulin, and lipids along with adipokines were measured. Insulin resistance was measured from homeostatic measurement of insulin resistance and oral glucose tolerance test. Hepatic and visceral adipose tissue catalase, glutathione peroxidase activities were measured along with tissue lipid peroxidation. Hepatic and adipose gene expression was measured using quantitative PCR.Both HSD and HFD feeding induced visceral obesity, plasma triglycerides and insulin resistance to similar extent. Plasma monocyte chemoattractant protein (MCP) 1, interleukin (IL)‐10, adiponectin and leptin levels were increased to similar extent by HSD and HFD feeding. Though HSD and HFD feeding induced oxidative stress in liver and adipose tissue, HFD induced it to greater extent than that of HSD. Hepatic expression of genes related to lipid metabolism and inflammation were induced to similar extent by HSD and HFD feeding except E‐selectin and Il4 which were induced to greater extent by HFD. Both HSD and HFD‐diets induced genes related to inflammation and oxidative stress to similar extent in visceral adipose tissue, whereas 11β‐hydroxysteroid dehydrogenase (HSD) 1, enzyme involved in pre‐receptor metabolism of active glucocorticoids is only induced by HFD feeding.Here, we conclude that feeding high‐sucrose and high‐fructose diets induce metabolic syndrome risk factors including visceral obesity, dyslipidemia and insulin resistance to similar extent in Wister rats. Further, we propose that under the conditions of higher dietary carbohydrate intake, relatively similar levels of dietary sucrose can increase the risk of metabolic syndrome to similar extent like that of dietary fructose, though it contains less fructose. Further understanding amount of minimal fructose needed to metabolically program the animal towards MS development in presence of other monosaccharides greatly helps in understanding the biology of fructose‐induced metabolic syndrome.Support or Funding InformationThe present study was carried out with the financial support of Department of Biotechnology (DBT), Ministry of Science and Technology, Government of India, and Indian Council of Medical Research (ICMR), Government of India. AS was supported by Fellowship from Council of Scientific and Industrial Research (CSIR).This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.