Abstract

Background. Increased fructose consumption is linked to the development of metabolic syndrome (MS). Here we investigated the time course of development of MS features in high-fructose-fed Sprague Dawley rats along with circulatory testosterone and homocysteine levels. Methods. Rats were divided into control and experimental groups and fed with diets containing 54.5% starch and fructose, respectively, for 4, 12, and 24 weeks. Plasma testosterone and homocysteine levels were measured along with insulin, glucose, and lipids. Body composition, insulin resistance, and hepatic lipids were measured. Results. Increase in hepatic triglyceride content was first observed in metabolic disturbance followed by hypertriglyceridemia and systemic insulin resistance in fructose-fed rats. Hepatic lipids were increased in time-dependent manner by fructose-feeding starting from 4 weeks, but circulatory triglyceride levels were increased after 12 weeks. Fasting insulin and Homeostatis Model Assessment of Insulin Resistance (HOMA-IR) were increased after 12 weeks of fructose-feeding. Decreased visceral adiposity, circulatory testosterone, and homocysteine levels were observed after 4 weeks of fructose-feeding, which were normalized at 12 and 24 weeks. Conclusions. We conclude that transient decrease in circulatory testosterone and homocysteine levels and increased hepatic triglyceride content are the earliest metabolic disturbances that preceded hypertriglyceridemia and insulin resistance in fructose-fed SD rats.

Highlights

  • Increased fructose consumption is linked to the development of metabolic syndrome (MS)

  • We investigated the sequential development of MS risk factors including fatty liver, insulin resistance, dyslipidemia, and visceral adiposity by feeding high-fructose diet (54.5%) for different durations to Sprague Dawley rats, one of the extensively used rat strain for fructose-induced MS experiments

  • Oil red O staining further confirmed the increase in hepatic lipid content in fructose-fed rats compared with that of control rats (Figures 1(a), 1(b), and 1(c))

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Summary

Introduction

Increased fructose consumption is linked to the development of metabolic syndrome (MS). Increase in hepatic triglyceride content was first observed in metabolic disturbance followed by hypertriglyceridemia and systemic insulin resistance in fructose-fed rats. We conclude that transient decrease in circulatory testosterone and homocysteine levels and increased hepatic triglyceride content are the earliest metabolic disturbances that preceded hypertriglyceridemia and insulin resistance in fructose-fed SD rats. MS is a complex pathophysiological entity characterized by insulin resistance (IR), central obesity, hypertension, and dyslipidemia [4] Both genetic factors and environmental factors like sedentary lifestyle and high calorie intake result in MS development [4]. Fructose consumption is positively associated with dyslipidemia, insulin resistance, and obesity [6, 7] These observations are further supported by animal studies, where feeding of fructose-rich diets resulted in all features of MS [8]. Majority of the studies on fructose-induced MS are single time point studies

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