‘Famine survival gene’ offers clues to cause of obesity

LONDON - Apart from junk food, desk jobs, and inactivity, there is one more thing behind those unwanted pounds - our genome, which has apparently not caught up with the fact that we no longer live in the Stone Age, suggests a new study.

Researchers at the Salk Institute for Biological Studies have shown that mice lacking a gene regulating energy balance are protected from weight gain, even on a high fat diet.

These findings have implications for the worldwide obesity epidemic and its consequences, such as type two diabetes.

“Ideas about obesity are based on concepts of feast or famine. As humans, we developed ways of coping with famine by expressing genes like CRTC3 to slow the rate of fat burning. Individuals with these active “thrifty genes” had an advantage-they could survive long periods without food,” said Marc Montminy, lead author of the study.

To examine the its role in fat metabolism, the researchers engineered mice lacking the CRTC3 gene and put them on diets of varying fat composition. Normal and CRTC3 gene “knockout” mice appeared similar when fed a moderate fat diet. But when fed the mouse version of the Philly cheese steak diet, only the normal mice became obese.

“The CRTC3 knockout mice were leaner and protected from obesity. They also had about twice as many brown fat cells than did normal mice,” said Montminy.

In fact, some evidence has also suggested that humans with a genetic propensity to leanness have more brown fat cells than do “ample” individuals. As desirable as that trait may seem in a “super-size me” world, those folks likely had a pretty tough time in the Paleolithic era.

Although the researchers found that CRTC3 loss also perturbs how all fat cells respond to brain signals controlling energy expenditure, they remain particularly intrigued by the brown fat connection.

The findings were published in the journal Nature. (ANI)