Sucrose induces fatty liver and pancreatic inflammation in male breeder rats independent of excess energy intake

Metabolism. 2011 Sep;60(9):1259-70. doi: 10.1016/j.metabol.2011.01.008. Epub 2011 Apr 12.

Abstract

Fructose induces metabolic syndrome in rats; but studies have been criticized for using high concentrations of fructose that are not physiologic, for using only pure fructose, and for not controlling for energy intake. We tested the hypothesis that a 40% sucrose diet (containing 20% fructose) might induce features of metabolic syndrome in male breeder rats independent of excess energy intake. Male Sprague-Dawley breeder rats were pair fed 40% sucrose or isocaloric starch diet for 4 months and evaluated for metabolic syndrome and diabetes. In vitro studies were performed in rat insulinoma cells (RIN-m5F) exposed to uric acid, and markers of inflammation were assessed. Rats fed a 40% sucrose diet developed accelerated features of metabolic syndrome with up-regulation of fructose-dependent transporter Glut5 and fructokinase. Fatty liver and low-grade pancreatic inflammation also occurred. Uric acid was found to stimulate inflammatory mediators and oxidative stress in islet cells in vitro. Sucrose, at concentrations ingested by a subset of Americans, can accelerate metabolic syndrome, fatty liver, and type 2 diabetes mellitus in male breeder rats; and the effects are independent of excess energy intake.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anion Transport Proteins / genetics
  • Cell Line, Tumor
  • Energy Intake*
  • Fatty Liver / etiology*
  • Fructose / metabolism
  • Male
  • Metabolic Syndrome / etiology
  • Pancreatitis / etiology*
  • Rats
  • Rats, Sprague-Dawley
  • Starch / administration & dosage
  • Sucrose / administration & dosage
  • Sucrose / toxicity*

Substances

  • Anion Transport Proteins
  • URAT1 protein, rat
  • Fructose
  • Sucrose
  • Starch