Thiazolidinediones and the promise of insulin sensitization in type 2 diabetes

Cell Metab. 2014 Oct 7;20(4):573-91. doi: 10.1016/j.cmet.2014.08.005. Epub 2014 Sep 18.

Abstract

Type 2 diabetes is caused by insulin resistance coupled with an inability to produce enough insulin to control blood glucose, and thiazolidinediones (TZDs) are the only current antidiabetic agents that function primarily by increasing insulin sensitivity. However, despite clear benefits in glycemic control, this class of drugs has recently fallen into disuse due to concerns over side effects and adverse events. Here we review the clinical data and attempt to balance the benefits and risks of TZD therapy. We also examine potential mechanisms of action for the beneficial and harmful effects of TZDs, mainly via agonism of the nuclear receptor PPARγ. Based on critical appraisal of both preclinical and clinical studies, we discuss the prospect of harnessing the insulin sensitizing effects of PPARγ for more effective, safe, and potentially personalized treatments of type 2 diabetes.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Cardiovascular Diseases / drug therapy
  • Diabetes Mellitus, Type 2 / drug therapy*
  • Edema / etiology
  • Fractures, Bone / drug therapy
  • Humans
  • Hypoglycemic Agents / adverse effects
  • Hypoglycemic Agents / therapeutic use*
  • Insulin / metabolism*
  • Non-alcoholic Fatty Liver Disease / drug therapy
  • PPAR gamma / agonists
  • PPAR gamma / metabolism
  • Thiazolidinediones / adverse effects
  • Thiazolidinediones / therapeutic use*
  • Urinary Bladder Neoplasms / drug therapy

Substances

  • Hypoglycemic Agents
  • Insulin
  • PPAR gamma
  • Thiazolidinediones