Taurine exerts hypoglycemic effect in alloxan-induced diabetic rats, improves insulin-mediated glucose transport signaling pathway in heart and ameliorates cardiac oxidative stress and apoptosis

Toxicol Appl Pharmacol. 2012 Jan 15;258(2):296-308. doi: 10.1016/j.taap.2011.11.009. Epub 2011 Nov 26.

Abstract

Hyperlipidemia, inflammation and altered antioxidant profiles are the usual complications in diabetes mellitus. In the present study, we investigated the therapeutic potential of taurine in diabetes associated cardiac complications using a rat model. Rats were made diabetic by alloxan (ALX) (single i.p. dose of 120mg/kg body weight) and left untreated or treated with taurine (1% w/v, orally, in water) for three weeks either from the day of ALX exposure or after the onset of diabetes. Animals were euthanized after three weeks. ALX-induced diabetes decreased body weight, increased glucose level, decreased insulin content, enhanced the levels of cardiac damage markers and altered lipid profile in the plasma. Moreover, it increased oxidative stress (decreased antioxidant enzyme activities and GSH/GSSG ratio, increased xanthine oxidase enzyme activity, lipid peroxidation, protein carbonylation and ROS generation) and enhanced the proinflammatory cytokines levels, activity of myeloperoxidase and nuclear translocation of NFκB in the cardiac tissue of the experimental animals. Taurine treatment could, however, result to a decrease in the elevated blood glucose and proinflammatory cytokine levels, diabetes-evoked oxidative stress, lipid profiles and NFκB translocation. In addition, taurine increased GLUT 4 translocation to the cardiac membrane by enhanced phosphorylation of IR and IRS1 at tyrosine and Akt at serine residue in the heart. Results also suggest that taurine could protect cardiac tissue from ALX induced apoptosis via the regulation of Bcl2 family and caspase 9/3 proteins. Taken together, taurine supplementation in regular diet could play a beneficial role in regulating diabetes and its associated complications in the heart.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alloxan
  • Animals
  • Apoptosis / drug effects
  • Biological Transport / drug effects
  • Diabetes Mellitus, Experimental / drug therapy*
  • Diabetes Mellitus, Experimental / physiopathology
  • Glucose / metabolism*
  • Glucose Transporter Type 4 / metabolism
  • Heart / drug effects
  • Insulin / metabolism*
  • Lipids / blood
  • Male
  • NF-kappa B / metabolism
  • Oxidative Stress / drug effects*
  • Protein Transport / drug effects
  • Rats
  • Rats, Wistar
  • Signal Transduction / drug effects
  • Taurine / pharmacology*

Substances

  • Glucose Transporter Type 4
  • Insulin
  • Lipids
  • NF-kappa B
  • Taurine
  • Alloxan
  • Glucose