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Thiazolidinediones and the preservation of β‐cell function, cellular proliferation and apoptosis
Author(s) -
Decker Michael,
Hofflich Heather,
Elias Alan N.
Publication year - 2008
Publication title -
diabetes, obesity and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.445
H-Index - 128
eISSN - 1463-1326
pISSN - 1462-8902
DOI - 10.1111/j.1463-1326.2007.00745.x
Subject(s) - diabetes mellitus , type 2 diabetes , beta cell , cell growth , insulin resistance , apoptosis , medicine , insulin , type 2 diabetes mellitus , cell , endocrinology , cancer research , bioinformatics , biology , biochemistry , islet
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.