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University of Maryland School of Medicine Researchers Find Common Drug Mimics Anti-Diabetes Effects of Bariatric Surgery

Tuesday, June 19, 2012

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 Researchers Steven D. Munger, Ph.D., and Mark A. Rizzo, Ph.D. conducted the study.
 

Researchers at the University of Maryland School of Medicine have found that the anti-diabetes effects of bariatric surgeries might be mimicked, at least in part, by a common medicine. Their results were just published in the American Journal of Physiology – Endocrinology and Metabolism.

Scientists have long observed that bariatric surgeries used to control weight — particularly the Roux-en-Y gastric bypass procedure — seem to affect diabetes. In fact, many Roux-en-Y patients who have Type 2 diabetes before surgery see their diabetes disappear within days of the surgery. This effect is so dramatic that some doctors are considering Roux-en-Y as a surgical treatment for diabetes.

The reason for this effect has not been clear, but one leading hypothesis – called the “hindgut hypothesis” is that the surgery results in the increase of an anti-diabetes factor from the lower gut. The leading candidate for this factor that fights diabetes is the gut hormone GLP-1. A major action of GLP-1 is to increase insulin production from the pancreas, thus lowering blood glucose levels. But until now, doctors haven’t understood why GLP-1 secretion would increase after Roux-en-Y.

The new preclinical study from University of Maryland School of Medicine researchers shows that Roux-en-Y surgery unmasks a novel glucose-sensing mechanism in the large intestine of rodents that promotes robust GLP-1 secretion. This mechanism can be engaged by a common drug (glibenclamide) even without surgery. Researchers believe they might be able to mimic some of the anti-diabetes effects of Roux-en-Y surgery with this common medication, glibenclamide.

The study examines the molecular mechanisms by which the body responds to sugars and sweeteners once they are eaten. The researchers also uncovered important new insights into how sweet taste receptors found in the intestine and pancreas participate in hormone responses to sugars.

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