Cardiac function and metabolism in Type 2 diabetic mice after treatment with BM 17.0744, a novel PPAR-alpha activator

Am J Physiol Heart Circ Physiol. 2002 Sep;283(3):H949-57. doi: 10.1152/ajpheart.00226.2001.

Abstract

Hearts from diabetic db/db mice, a model of Type 2 diabetes, exhibit left ventricular failure and altered metabolism of exogenous substrates. Peroxisome proliferator-activated receptor-alpha (PPAR-alpha) ligands reduce plasma lipid and glucose concentrations and improve insulin sensitivity in db/db mice. Consequently, the effect of 4- to 5-wk treatment of db/db mice with a novel PPAR-alpha ligand (BM 17.0744; 25-38 mg x kg(-1) x day(-1)), commencing at 8 wk of age, on ex vivo cardiac function and metabolism was determined. Elevated plasma concentrations of glucose, fatty acids, and triacylglycerol (34.0 +/- 3.6, 2.0 +/- 0.4, and 0.9 +/- 0.1 mM, respectively) were reduced to normal after treatment with BM 17.0744 (10.8 +/- 0.6, 1.1 +/- 0.1, and 0.6 +/- 0.1 mM). Plasma insulin was also reduced significantly in treated compared with untreated db/db mice. Chronic treatment of db/db mice with the PPAR-alpha agonist resulted in a 50% reduction in rates of fatty acid oxidation, with a concomitant increase in glycolysis (1.7-fold) and glucose oxidation (2.3- fold). Correction of the diabetes-induced abnormalities in systemic and cardiac metabolism after BM 17.0744 treatment did not, however, improve left ventricular contractile function.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blood Glucose / metabolism
  • Diabetes Mellitus, Type 2 / drug therapy*
  • Diabetes Mellitus, Type 2 / metabolism
  • Diabetes Mellitus, Type 2 / physiopathology
  • Disease Models, Animal
  • Fatty Acids, Nonesterified / blood
  • Female
  • Glycolysis
  • Hyperglycemia / drug therapy
  • Hyperglycemia / metabolism
  • Hyperglycemia / physiopathology
  • Insulin / blood
  • Lauric Acids / pharmacology*
  • Mice
  • Mice, Inbred C57BL
  • Mice, Mutant Strains
  • Myocardium / metabolism*
  • Oxidation-Reduction
  • Palmitates / metabolism
  • Receptors, Cytoplasmic and Nuclear / metabolism*
  • Transcription Factors / metabolism*
  • Triglycerides / blood
  • Ventricular Function, Left / physiology*

Substances

  • 2,2-dichloro-12-(p-chlorophenyl)-dodecanoic acid
  • Blood Glucose
  • Fatty Acids, Nonesterified
  • Insulin
  • Lauric Acids
  • Palmitates
  • Receptors, Cytoplasmic and Nuclear
  • Transcription Factors
  • Triglycerides