(Ivanhoe Newswire) — It turns out our ancient ancestors may be to blame for the obesity epidemic. According to a research team at the Salk Institute of Biological Studies, evolutionary adaptations may have genetically shaped how our body stores and burns fat.
Led by Marc Montminy, M.D., Ph.D, and professor at the Clayton Foundation Laboratories for Peptide Biology, the team studied a particular gene called CRT3, which is responsible for decreasing energy expenditure in fat cells.
“Ideas about obesity are based on concepts of feast or famine,” Montminy was quoted as saying. “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 ‘thrift genes’ had an advantage – they could survive long periods without food.”
The idea of metabolism-slowing “thrifty genes” dates back to the 1960’s, having been developed before the concept of genome sequencing, but this study breathes new life into it.
To study the CRTC3 gene, the scientists genetically engineered test mice to lack it. They then put the CRTC3-free mice on diets with varying amounts of fat content and compared them to a set of normal control mice. They found little variance when both groups were fed a moderate fat diet, but were surprised to find that only the control mice became obese after consuming a Philly cheese steak diet.
“The CRTC3 knockout mice were leaner and protected from obesity,” Montminy was quoted as saying. “They also had about twice as many brown fat cells than did normal mice.”
The distinction between brown fat (BAT) and the less desirable white fat (WAT) is important to make. Brown fat tissue is “good fat,” responsible for generating heat and maintaining body temperature. It does so by burning the waistline-expanding WAT, which accumulates around the waistline and hips.
“CRTC3 could be a switch controlling the number of brown fat cells,” Montminy was quoted as saying. “That is key, because if you could make more brown adipocytes, you could potentially control obesity.”
Montminy and his team found a mutation of CRTC3, which appeared to be more potent than a normal CRTC3 in its affects. Since the mice in the study who lacked the gene were better able to fight obesity, the researchers believed that this amped-up version of the gene would put individuals at a higher risk of obesity.
After collecting information from genetic databases at the Cedars-Sinai Medical Center in Los Angeles, the theory proved to be a promising one. Looking at two groups of Mexican-American patients, one with the mutation and the other without, the researchers found that the individuals in the CRTC3 mutation group were more likely to be obese.
“This is an example in which findings from rodent research led to a novel discovery in humans,” Cedars- Sinai endocrinologist and study collaborator Mark Goodarzi, M.D., Ph.D, was quoted as saying. “Not all Mexican American individuals with the variant will develop obesity, but those carrying it are at higher risk.”
SOURCE: Salk Institute, December 2010
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