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High-carbohydrate High-fat Diet–induced Metabolic Syndrome and Cardiovascular Remodeling in Rats

Panchal, Sunil K MSc*; Poudyal, Hemant MBiotech; Iyer, Abishek MMolBiol; Nazer, Reeza BSc; Alam, Ashraful MSc; Diwan, Vishal MPharm; Kauter, Kathleen PhD*; Sernia, Conrad PhD; Campbell, Fiona PhD; Ward, Leigh PhD§; Gobe, Glenda PhD; Fenning, Andrew PhD; Brown, Lindsay PhD*†

Journal of Cardiovascular Pharmacology: January 2011 - Volume 57 - Issue 1 - p 51-64
doi: 10.1097/FJC.0b013e3181feb90a
Original Article

The prevalence of metabolic syndrome including central obesity, insulin resistance, impaired glucose tolerance, hypertension, and dyslipidemia is increasing. Development of adequate therapy for metabolic syndrome requires an animal model that mimics the human disease state. Therefore, we have characterized the metabolic, cardiovascular, hepatic, renal, and pancreatic changes in male Wistar rats (8-9 weeks old) fed on a high-carbohydrate, high-fat diet including condensed milk (39.5%), beef tallow (20%), and fructose (17.5%) together with 25% fructose in drinking water; control rats were fed a cornstarch diet. During 16 weeks on this diet, rats showed progressive increases in body weight, energy intake, abdominal fat deposition, and abdominal circumference along with impaired glucose tolerance, dyslipidemia, hyperinsulinemia, and increased plasma leptin and malondialdehyde concentrations. Cardiovascular signs included increased systolic blood pressure and endothelial dysfunction together with inflammation, fibrosis, hypertrophy, increased stiffness, and delayed repolarization in the left ventricle of the heart. The liver showed increased wet weight, fat deposition, inflammation, and fibrosis with increased plasma activity of liver enzymes. The kidneys showed inflammation and fibrosis, whereas the pancreas showed increased islet size. In comparison with other models of diabetes and obesity, this diet-induced model more closely mimics the changes observed in human metabolic syndrome.

From the *Department of Biological and Physical Sciences, University of Southern Queensland, Toowoomba, Queensland, Australia; †School of Biomedical Sciences, ‡School of Veterinary Science, §School of Chemistry and Molecular Biosciences, and ¶Centre for Kidney Disease Research, School of Medicine, The University of Queensland, Brisbane, Queensland, Australia; and ‖Faculty of Sciences, Engineering and Health, Central Queensland University, Rockhampton, Queensland, Australia.

Received for publication April 2, 2010; accepted September 26, 2010.

Supported partially by grants from The Prince Charles Hospital Foundation, Brisbane, Queensland, Australia.

We thank Mr. Greg Jardine, Dr. Red Nutraceuticals, Mt. Nebo, Queensland, Australia, for financial support to allow this project to be undertaken.

The authors report no conflicts of interest.

Reprints: Lindsay Brown, PhD, Department of Biological and Physical Sciences, University of Southern Queensland, Toowoomba, Queensland 4350, Australia (e-mail:

© 2011 Lippincott Williams & Wilkins, Inc.