The most award winning
healthcare information source.
TRUSTED FOR FOUR DECADES.
What if your patients could eat all they like and take a little pill to suppress genes that trigger insulin resistance and weight gain?
Sound like a dream?
That little pill may still be a decade or more away, but important new findings from the Merck-Frosst Center for Therapeutic Research in Pointe Claire-Dorval, Quebec have turned attention toward suppression of the gene protein tyrosine phosphatase-1B (PTP-1B) as the wave of the future of treatment of diabetes.
Lead researcher Brian Kennedy, PhD, a molecular biologist and senior research fellow at Merck-Frosst says the discovery "will open a whole new area of diabetes research. I have a pretty good feeling this may be the underlying cause of resistance in Type 2 diabetes."
His excitement is mirrored on a slightly less enthusiastic level by Harvey Ketzeff, MD, chief of the division of Endocrinology at Long Island Jewish Medical Center in New Hyde Park, NY.
"This is further evidence that genetic influences are critical in the development of diabetes and obesity," Ketzeff said. "There are many genes involved in insulin action, but understanding how this gene works will help us learn how to become sensitive to insulin."
Kennedy’s research team was able to remove the PTP-1B gene by using altered stem cells in a tissue culture in mice. The altered mice and a control group were fed the same high-fat high-calorie diet.
"In the fed state, PTP-1B mice had a significant 13% reduction in blood glucose concentrations. . . . The PTP-1B mice had circulating insulin concentrations that were about half those of the control-fed animals." Kennedy wrote in the study published in Science on March 5.
Kennedy said he was surprised to find the mice did not gain weight. "During the 10 weeks the mice were on this diet, male and female wild-type littermates rapidly gained weight, whereas PTP-1B mice were substantially protected from diet-induced weight gain."
"I wouldn’t be surprised if some people are genetically protected against diabetes and obesity," Kennedy says. "This is the first time there has been such a link found and it’s a good target to develop drugs against."
[Contact Brian Kennedy at (514) 695-8221.]