Volume 10, Issue 8 p. 617-625

Thiazolidinediones and the preservation of β-cell function, cellular proliferation and apoptosis

Michael Decker

Michael Decker

Department of Medicine, University of California, Irvine, Medical Center, Orange, CA, USA

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Heather Hofflich

Heather Hofflich

Department of Medicine, University of California, Irvine, Medical Center, Orange, CA, USA

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Alan N. Elias

Corresponding Author

Alan N. Elias

Department of Medicine, University of California, Irvine, Medical Center, Orange, CA, USA

Alan N. Elias, MD, Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, UCI Medical Center, 101 The City Drive South, Orange, CA 92868, USA.
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First published: 10 July 2008
Citations: 17

Abstract

The thiazolidinediones (TZDs) or glitazones are pharmaceutical agents that have profound effects on energy expenditure and conservation. They also exert significant anti-inflammatory effects and influence cell proliferation and cell death. The drugs are primarily used in clinical practice in the treatment of patients with type 2 diabetes mellitus, a disorder of insulin resistance that occurs when the pancreatic β-cells are unable to produce adequate amounts of insulin to maintain euglycaemia. Loss of pancreatic β-cell function in type 2 diabetes is progressive and often precedes overt diabetes by 10 years or more, as was shown by the United Kingdom Prospective Diabetes Study. Any therapeutic or preventive approach that would limit or reverse loss of β-cell function in diabetes would have profound effects on the morbidity associated with this widespread disease. Evidence suggesting a potential role of TZDs in preserving β-cell function in type 2 diabetes as well as the ability of these agents to exert anti-inflammatory and proapoptotic anticancer effects, and their ability to promote cellular proliferation in various organs is reviewed.