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Diabetes Risk Hiked By Missing Sugar Molecule

by Tanya Thomas on  February 27, 2011 at 10:36 AM Diabetes News   - G J E 4
Scientists say that an evolutionary gene mutation that occurred in human millions of years ago and our subsequent inability to produce a specific kind of sugar molecule appears to make people more vulnerable to developing type 2 diabetes, especially if they're overweight.
 Diabetes Risk Hiked By Missing Sugar Molecule
Diabetes Risk Hiked By Missing Sugar Molecule
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The study was carried out by researchers at the University of California, San Diego School of Medicine and Rady Children's Hospital-San Diego.

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Jane J. Kim, corresponding study author from Rady Children's Hospital, said the findings represent the first documented evidence linking the sugar production to insulin and glucose metabolism problems associated with diabetes.

"Given the global epidemic of obesity and diabetes, we think that these findings suggest that evolutionary changes may have influenced our metabolism and perhaps increased our risk of the disease," Kim said.

Type 2 diabetes is caused by both genetic and environmental factors, such as a fatty diet and lack of exercise, that result in progressively dysfunctional pancreatic beta cells, elevated blood sugar levels due to insulin resistance and eventual health complications, sometimes fatally so.

Sialic acids are sugar molecules found on the surfaces of all animal cells, where they act as vital contact points for interaction with other cells and with their surrounding environment.

Virtually all mammals produce two types: N-acetylneuraminic acid (Neu5Ac) and N-glycolylneuraminic acid (Neu5Gc).

Humans are the exception. For reasons lost in the mists of evolution, a mutation in a gene called CMAH occurred 2 to 3 million years ago, inactivating an enzyme in humans that catalyzes production of Neu5Gc by adding a single oxygen atom to Neu5Ac.

Researchers compared two groups of mice: one with a functional CMAH gene, the other with an altered CMAH gene similar to the human mutation.

Both groups of mice were fed a high-fat diet. Mice in both groups became obese and developed insulin resistance. However, only mice with the CMAH gene mutation experienced pancreatic beta cell failure - the cells that make and release insulin, a hormone that controls blood sugar levels.

Kim said the findings help refine understanding of why obese humans appear to be particularly vulnerable to type 2 diabetes.

The study has been published in the Feb. 24 online edition of The FASEB Journal, a publication of the Federation of American Societies of Experimental Biology.

Source: ANI
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