Pancreatic islet response to hyperglycemia is dependent on peroxisome proliferator-activated receptor alpha (PPARalpha)

FEBS Lett. 2005 Apr 25;579(11):2284-8. doi: 10.1016/j.febslet.2005.03.020.

Abstract

This study tests the hypothesis that islet peroxisome proliferator-activated receptor alpha (PPARalpha) influences insulin secretion. Freshly isolated islets of normoglycemic PPARalpha-null mice display no major alteration of glucose-stimulated insulin release. However, after 24 h of culture in high glucose, PPARalpha-null islets exhibit elevated basal insulin secretion and fail to increase insulin mRNA. 24-h culture with palmitate replicates this phenotype in wild-type islets. The data suggest that PPARalpha is needed to ensure appropriate insulin secretory response in situation of short-term hyperglycemia, likely by maintaining islet lipid homeostasis. As such, islet PPARalpha could contribute to delay the progression of type 2 diabetes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animal Feed
  • Animals
  • Fats / pharmacology
  • Gene Expression Regulation
  • Glucose / pharmacology
  • Hyperglycemia / metabolism*
  • Insulin / genetics
  • Insulin / metabolism
  • Insulin Secretion
  • Islets of Langerhans / drug effects
  • Islets of Langerhans / metabolism*
  • Male
  • Mice
  • Mice, Knockout
  • PPAR alpha / deficiency
  • PPAR alpha / genetics
  • PPAR alpha / metabolism*
  • Tissue Culture Techniques

Substances

  • Fats
  • Insulin
  • PPAR alpha
  • Glucose