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'Obesity gene' involved in weight gain response to high-fat diet identified.


Byline: ANI

Washington, Feb 25 (ANI): A team of scientists, including an Indian-origin boffin bof·fin also Bof·fin  
n. Chiefly British Slang
A scientist, especially one engaged in research.



[Origin unknown.
, has identified a specific gene that plays a key role in the weight-gain response to a high-fat diet high-fat diet A diet rich in fats, often saturated–animal or tropical oils—fats Adverse effects Arthritis, CA, vascular disease, DM, HTN, obesity, stroke. See Fat, Fatty acids, Saturated fat acis, Cf Low-fat diet. .

The study, conducted on mice, has suggested that blocking this gene could one day be a therapeutic strategy to reduce diet-related obesity and associated disorders, such as diabetes and liver damage, in humans.

The researchers found that a diet rich in fat induced production of this gene, called protein kinase C Protein kinase C ('PKC', EC 2.7.11.13) is a family of protein kinases consisting of ~10 isozymes.[1] They are divided into three subfamilies: conventional (or classical), novel, and atypical based on their second messenger requirements.  beta (PKC PKC Protein Kinase C (biochemistry)
PKC Public Key Cryptography
PKC Public Key Certificate
PKC PaKua Chang (Chinese martial art)
PKC Paroxysmal Kinesigenic Choreoathetosis
 beta), in the fat cells of mice. These mice rapidly gained weight while eating a high-fat diet for 12 weeks.

On the other hand, mice genetically engineered to lack PKC beta gained relatively little weight and showed minimal health effects after eating the same high-fat diet.

In comparing the effects of the high-fat diet and a regular diet, the scientists found that mice fed the high-fat diet produced more PKC beta in their fat tissue than did mice eating a regular diet.

"So we now know this gene is induced by a high-fat diet in fat cells, and a deficiency of this gene leads to resistance to fat-induced obesity and related insulin resistance and liver damage," said Kamal Mehta, senior author of the study and a professor of molecular and cellular biochemistry in Ohio State University's College of Medicine.

"It could be that the high-fat diet is a signal to the body to store more fat. And when that gene is not there, then the fat storage cannot occur," Mehta added.

Mehta said that although the complete mechanism remains unknown, the research to date suggests that rather than storing fat, mice lacking the gene burn fat more rapidly than they would if the PKC beta were present.

Mehta and colleagues previously had created the hybrid mouse model by cross-breeding mice deficient in PKC beta with the C57 black mouse, a common animal used in research for studying diabetes and obesity.

Despite the propensity for obesity from their original genes, the new mice lost weight while eating up to 30 percent more food than other mice.

"Obesity leads to liver damage and to diabetes. So if we can take care of obesity associated with a high-fat diet, we can also take care of most of the related disorders. It is very likely that this gene may be involved in a predisposition to obesity," Mehta said.

The research is available online in the journal Hepatology and is scheduled for later print publication. (ANI)

Copyright 2009 Asian News International The Asian News International (ANI) agency provides multimedia news to China and 50 bureaus in India. It covers virtually all of South Asia since its foundation and presently claims, on its official website, to be the leading South Asia-wide news agency.  (ANI) - All Rights Reserved.

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Publication:Asian News International
Date:Feb 25, 2009
Words:433
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