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Rosiglitazone promotes PPARγ-dependent and -independent alterations in gene expression in mouse islets

Hannah J Welters1, Abdelfattah El Ouaamari, Dan Kawamori

  • 1Peninsula College of Medicine and Dentistry, University of Exeter, Exeter EX2 5DW, United Kingdom. hannah.welters@pcmd.ac.uk.

Endocrinology
|July 19, 2012
PubMed

Insights

Peroxisome proliferator-activated receptor gamma (PPARγ) in pancreatic beta cells is not essential for rosiglitazone

Area of Science:

  • Endocrinology and Metabolism
  • Molecular Biology

Background:

  • Glitazones are insulin-sensitizing agents that activate peroxisome proliferator-activated receptor gamma (PPARγ) in adipocytes.
  • The role of PPARγ within pancreatic beta cells regarding their function and drug responses remains unclear.

Purpose of the Study:

  • To investigate the in vivo necessity of PPARγ expression in adult beta cells for mediating the effects of rosiglitazone.
  • To determine if PPARγ in beta cells is crucial for beta-cell sparing properties and insulin sensitivity.

Main Methods:

  • Generated an inducible Cre-loxP system to specifically knockout PPARγ in adult beta cells (PPARgKO mice).
  • Assessed glucose homeostasis, insulin sensitivity, and beta-cell function (secretion, size, proliferation) under normal and high-fat diet conditions.
  • Administered rosiglitazone to evaluate its efficacy in both wild-type and PPARgKO mice.

Main Results:

  • PPARγ knockout in beta cells (PPARgKO) did not significantly alter glucose or insulin sensitivity on a chow or high-fat diet.
  • Rosiglitazone treatment failed to improve insulin sensitivity or beta-cell function in PPARgKO mice compared to controls.
  • Islet size and proliferation remained unchanged in PPARgKO mice, irrespective of diet or drug treatment.

Conclusions:

  • Beta-cell expression of PPARγ is not essential for the insulin-sensitizing actions of rosiglitazone.
  • PPARγ in beta cells does not appear to play a direct role in maintaining normal beta-cell function or proliferation.

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