Lack of enzyme turns fat cells
into fat burners
January 24, 2005
Lack of the enzyme, acetyl CoA carboxylase 2 or ACC2,
appears to turn the adipose or fat cells of mice into
fat burners, explaining in part why the animals can
eat more and weigh less than their normal counterparts,
said Baylor College of Medicine researchers.
The report that appears online today in the Proceedings
of the National Academy of Sciences.
"We 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 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.
Source:www.eurekalert.org
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