Peroxisome proliferator-activated receptor (PPAR)-alpha activation prevents diabetes in OLETF rats: comparison with PPAR-gamma activation

Diabetes. 2003 Sep;52(9):2331-7. doi: 10.2337/diabetes.52.9.2331.

Abstract

Lipid accumulation in nonadipose tissues is closely related to the development of type 2 diabetes in obese subjects. We examined the potential preventive effect of peroxisome proliferator-activated receptor (PPAR)-alpha and PPAR-gamma stimulation on the development of diabetes in obese diabetes-prone OLETF rats. Chronic administration of a PPAR-alpha agonist (0.5% [wt/wt] fenofibrate) or a PPAR-gamma agonist (3 mg x kg(-1) x day(-1) rosiglitazone) completely prevented the development of glycosuria. Pancreatic islets from untreated OLETF rats underwent sequential hypertrophy and atrophy, which was completely prevented by chronic fenofibrate treatment. In contrast, rosiglitazone treatment did not affect islet hypertrophy at earlier stages but prevented beta-cell atrophy at later stages. Fenofibrate treatment decreased body weight and visceral fat, whereas rosiglitazone treatment increased body weight. Despite the opposite effects on adiposity, both drugs were equally effective in improving insulin actions in skeletal muscle. Furthermore, both drugs significantly decreased the triglyceride content in the soleus muscle and pancreatic islets. The present study demonstrates that the PPAR-alpha agonist fenofibrate prevents the development of diabetes in OLETF rats by reducing adiposity, improving peripheral insulin action, and exerting beneficial effects on pancreatic beta-cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipose Tissue / drug effects
  • Adipose Tissue / pathology
  • Animals
  • Basal Metabolism / drug effects
  • Blood Glucose / metabolism
  • Diabetes Mellitus / drug therapy*
  • Diabetes Mellitus / pathology
  • Diabetes Mellitus, Type 2 / drug therapy
  • Diabetes Mellitus, Type 2 / pathology
  • Diabetes Mellitus, Type 2 / prevention & control*
  • Fatty Acids / metabolism
  • Fenofibrate / pharmacology*
  • Glycogen / biosynthesis
  • Hypoglycemic Agents / pharmacology
  • Hypolipidemic Agents / pharmacology*
  • Insulin / pharmacology
  • Islets of Langerhans / drug effects
  • Islets of Langerhans / metabolism
  • Islets of Langerhans / pathology
  • Male
  • Muscle, Skeletal / metabolism
  • Obesity*
  • Rats
  • Rats, Inbred OLETF
  • Receptors, Cytoplasmic and Nuclear / metabolism*
  • Rosiglitazone
  • Thiazoles / pharmacology
  • Thiazolidinediones*
  • Transcription Factors / metabolism*
  • Triglycerides / metabolism
  • Viscera

Substances

  • Blood Glucose
  • Fatty Acids
  • Hypoglycemic Agents
  • Hypolipidemic Agents
  • Insulin
  • Receptors, Cytoplasmic and Nuclear
  • Thiazoles
  • Thiazolidinediones
  • Transcription Factors
  • Triglycerides
  • Rosiglitazone
  • Glycogen
  • Fenofibrate