Researchers discover molecular 'switch' that tells body to store or burn fat

cids. Co-author Ntambi and colleagues originally cloned the SCD-1 gene in 1988 together with M. Daniel Lane, Ph.D., at Johns Hopkins University.

"SCD-1 has since been found to be very important for the synthesis of oleate despite the fact that mammalian diets supply abundant dietary oleate," says Ntambi, professor of biochemistry and nutritional sciences at the University of Wisconsin at Madison.

The next question the researchers asked was: to what extent does repression of SCD-1 contribute to leptin's actions?

They hypothesized that if suppression of SCD-1 is required for leptin action, then a mouse lacking SCD-1 should mimic some of leptin's effects. The researchers crossed leptin-deficient (ob/ob) mice with a mouse strain called "asebia," which carries mutations in the SCD-1 gene. The fatty acids that SCD-1 synthesizes are also required for normal function of sebaceous glands, so its absence leads to the "absence of sebaceous glands," hence the name "asebia." Sebaceous glands are embedded in the skin over most of the body and are more concentrated in the scalp, face, forehead and eyes. In the absence of sebaceous glands, mice have patchy, abnormal skin and abnormal corneas.

The researchers found that, similar to leptin treatment, removing SCD-1 markedly reduces the weight of the obese mouse at 16 weeks of age, weight was reduced by 29 percent in females and 34 percent in males. The reduced weight of these animals could be accounted for by a dramatic increase in energy expenditure. Indeed, removing SCD-1 completely corrected the effects of leptin deficiency on energy expenditure.

"The repression of SCD-1 accounts for a significant proportion, perhaps even all, of the effects of leptin on energy expenditure," says Friedman. "SCD-1 may act like a switch to control fat storage. When SCD-1 is 'up,' the switch is flipped in the direction of storing fat, and when it's 'down,' the switch is flipped in the direction of burning fa

Contact: Joseph Bonner
Rockefeller University

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