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Elimination of enzyme turns fat cells into fat burners

by Ruth SoRelle, MPH

Salih Wakil, PhD

When an enzyme called acetyl CoA carboxylase 2 or ACC2 is "knocked out" of the cells of specially bred mice, their fat cells become fat burners, said researchers at Baylor College of Medicine in a recently published paper in the Proceedings of the National Academy of Sciences.

That explains why these mice can eat more and weigh less than their normal counterparts, said Salih Wakil, PhD, chair of the BCM department of biochemistry and molecular biology.

"We studied the fat cells in these mice bred to lack ACC2," said Wakil "We found that the adipose in the mutant mice are now oxidizing fat, hydrolyzing (breaking down using water) fat, and passing it on to the heart and muscle because there is an increase in oxidation of fat in those organs. It also starts oxidizing glucose. In other words, the adipose tissue is becoming a little more oxidative and less involved in the synthesis and storage of fat. We feel this contributes to the status of the animal."

That status, as shown in prior studies by Wakil and his colleagues, is the ability to eat a high fat, high carbohydrate diet without gaining weight. In contrast, their normal counterparts who have ACC2 in their makeup become obese and even develop type 2 diabetes.

"This adds another tissue or organ that helps out in the process of energy maintenance," said Wakil. "ACC2 is potentially a key enzyme in the regulation of weight, obesity, and related problems."

Wakil and his colleagues studied the oxidation of fatty acid and glucose in cultures of fat cells isolated from both normal and mutant mice that lacked ACC2. When the mice were fed a normal diet, fatty acid oxidation was 80 percent higher in the fat cells of the mice lacking ACC2 that in the fat cells of the normal mice who had the gene. When fed a high fat, high carbohydrate diet for four to five months, the ACC2-deficient mice had a 25 percent higher rate of fatty acid oxidation and twofold higher rate of glucose oxidation than the normal mice.

Others who participated in the research included Drs. WonKeun Oh, Lutfi Abu-Elheiga, Parichher Kordari, Zeiwei Gu, Tattym Shaikenov, Subrahmanyam S. Chirala.

The work was supported in part by by the Clayton Foundation for Research and the National Institutes of Health.

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