Obesity could be in your genes

In a finding that could bring hope to millions, scientists have determined that a specific gene plays a role in the weight-gain response to a high-fat diet. The study conducted on mice found out that blocking this gene -- called Protein Kinase C beta or PKC beta -- helps reduce diet-related obesity and associated disorders like diabetes and liver damage.

"When this gene is absent, instead of storing it, the body burns fat and gets rid of it," said Kamal Mehta, senior author of the study and a professor of molecular and cellular biochemistry in Ohio State University's College of Medicine. "PKC beta might have helped humans when they were hunters, when the body needed to retain fat for survival," he added.

The studies found that a fat-rich diet induced PKC beta production in mice's fat cells. These mice rapidly gained weight while eating a high-fat diet for 12 weeks. The researchers then removed the gene from some mice and fed them with a high-fat diet -- they did not gain much weight and showed minimal health effects too.

The scientists found that mice eating high-fat diet produced more PKC beta in their fat tissue than mice eating a regular diet did.

"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," Mehta said. "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, the fat storage cannot occur."

Though the complete mechanism remains unknown, the research suggests that rather than storing fat, mice lacking PKC beta burnt fat more rapidly than they would if the gene was present, Mehta said.

The research is available online in the journal Hepatology. Co-authors on the paper were Wei Huang and Rishipal Bansode of the Department of Molecular and Cellular Biochemistry, and Madhu Mehta of the Department of Internal Medicine, all at Ohio State.

"It is very likely that this gene may be involved in a predisposition to obesity," Mehta said. The livers of the normal mice on high fat-diet were on average about 50 percent larger than the livers in mice lacking PKC beta. The gene-deficient mice were able to clear insulin to regulate blood sugar more rapidly than normal mice after eating the high-fat diet. It means avoiding obesity also allowed them to avoid development of insulin resistance associated with diabetes, said Mehta, also an investigator in Ohio State's Davis Heart and Lung Research Institute.

"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," Mehta said, adding that so far, mouse models have not shown any damaging side effects related to the suppression of PKC beta.