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New Approach Targets Gut Hormone to Lower Blood Sugars

Posted: Wednesday, August 12, 2009

A research team at the Toronto General Research Institute discovered a novel function of a hormone found in the gut that might potentially lower glucose levels in diabetes.  

In this ground-breaking study on a rat model, Dr. Lam's team discovered that activating receptors of the cholecystokinin (CCK) peptide hormone in the gut rapidly and potently lowers blood glucose levels by triggering a signal to the brain and then to the liver to lower glucose or sugar production. In the same experiment, CCK failed to lower blood glucose in rodents fed a high-fat diet for three days.
 
"Our findings reveal a novel role for the CCK hormone and suggest that CCK-resistance in the gut may contribute to high blood sugar levels in response to high-fat feeding in rodents. Understanding how to overcome CCK-resistance in the gut so that blood sugars can be lowered could be a novel therapeutic approach to diabetes and obesity," says Dr. Lam, who holds the John Kitson McIvor (1915 -- 1942) Chair in Diabetes Research at the Toronto General Research Institute and University of Toronto and is Assistant Professor in the Departments of Physiology and Medicine at the University of Toronto. "This paper compliments our study published last year in Nature indicating that, in the future, we may be able to design a drug to target the gut to lower glucose levels in patients with diabetes."
 
Dr. Lam stressed that the clinical therapeutic implications of the current findings remain largely unknown. A large amount of time will be required to determine whether enhancing CCK action in the gut of humans is effective and safe in lowering glucose levels in healthy individuals as well as patients with diabetes and obesity.
 
The research is published as the cover story in the August issue of Cell Metabolism. The paper is entitled, "Intestinal Cholecystokinin controls Glucose Production through a Neuronal Network".

Source: Diabetes In Control: Cell Metabolism, August, 2009-08-08

 
 
 
 
 
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