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Futile cycle both fights diabetes and causes weight gain

(Philadelphia, PA) If obesity is the leading cause of type II diabetes, then why do thiazolidinediones (TZDs), the only available drugs that treats this form of diabetes, actually cause more weight gain? online version of Nature Medicine, researchers at the University of Pennsylvania School of Medicine address the fundamental workings of TZDs (also known as glitazones or under brand names such as Actos and Avandia), and provide a potential new target for further study.

Their research describes how TZDs trigger the creation of glycerol kinase, an enzyme that causes fat cells to store fatty acids faster than it produces them.

"It is what researchers call a 'futile' cycle. Just as fat cells release their larder of fatty acids, glycerol kinase causes the fat cells to put them back in storage," said Mitchell A. Lazar, MD, PhD, Chief of the Division of Endocrinology, Diabetes, and Metabolism and Director of the Penn Diabetes Center. "The glycerol kinase is packing the pantry faster than fat cells can pull the cans off of the shelves. The net influx of fatty acids into fat tissue contributes to reduced fatty acids in the bloodstream that, in turn, leads to increased sensitivity to insulin."

Type II, or adult-onset diabetes, occurs as cells lose the ability to respond to insulin, a hormone which allows cells to absorb sugar for fuel. The disease affects millions, and has become an epidemic in the industrialized world. According to Lazar, two big mysteries remain concerning type II diabetes: how cells become insulin resistant and how TZDs cause them to lose resistance to insulin. By studying how the drug works, the researchers have uncovered a fundamental clue that may allow the development of better therapies "Right now, our findings suggest that weight gain is an inherent part of how TZDs function and diabetics should bear in mind the role of a healthy diet in combination with drug therapy," said Lazar. "TZDs actually lower insulin requirements in
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Contact: Greg Lester
lesterg@uphs.upenn.edu
215-349-5658
University of Pennsylvania School of Medicine
23-Sep-2002


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