studied the fat cells in these mice bred to lack ACC2," said Dr. Salih
Wakil, chair of the BCM department of biochemistry and molecular
biology. "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."
In prior studies, Wakil and his colleagues have demonstrated the effect
ACC2 has on mice. Mice bred to lack the enzyme can eat a high fat, high
carbohydrate diet without gaining weight, while their normal
counterparts become obese and 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 when compared to normal mice. When they were 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 O
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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