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