COLUMBUS, Ohio Scientists have determined that a specific gene plays a role in the weight-gain response to a high-fat diet.
The finding in an animal study suggests 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 beta (PKC 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."
Though 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 said.
The research is available online in the journal Hepatology and is scheduled for later print publication.
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 study
|Contact: Kamal Mehta|
Ohio State University