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Mice that are deficient in acetyl-CoA carboxylase are thinner than normal and exhibit continuous fatty acid...

Mice that are deficient in acetyl-CoA carboxylase are thinner than normal and exhibit continuous fatty acid oxidation. Explain these observations.

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Answer #1

Malonyl CoA generated by acetylCoA carboxylase (ACC) a key metabolite in the regulation of energy homeostasis. Here, we show that Acc2 −/− mutant mice have a normal life span, a higher fatty acid oxidation rate, and lower amounts of fat. In comparison to the wild type, Acc2-deficient mice had 10- and 30-fold lower levels of malonyl-CoA in heart and muscle, respectively. the fatty acid oxidation rate becomes higher than that of wild type for fulfulling its energy requirement.
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