When we have eaten well and take fat rich diet then in this condition Acetyl CoA produced from fatty acid breakdown will be gone to storage in adipose tissue or not? If it will go for storage then why and if not go for storage then what will be reason?

  • $\begingroup$ It may not be compulsory to store it. It should be converted into CO2 to yield energy. I don't think a few more ATP in the cell would hurt. $\endgroup$ May 22, 2016 at 15:50
  • $\begingroup$ But if cell has enough ATP then what will be fate of Acetyl CoA? $\endgroup$ May 22, 2016 at 15:56
  • $\begingroup$ respiration-related processes is not my field of research, so I'd just give a guess that yes, it'd be converted back to fatty acid & then stored. But, I don't think humans have ability to do so, so I'm not sure on this. $\endgroup$ May 22, 2016 at 15:59
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    $\begingroup$ This is either a trivial question, to which the answer is "If energy is needed then it will be used to generate ATP (in the liver) through the Krebs TCA cycle, if not it will be used to synthesize triglyceride (in the liver) which will be transported to the adipose tissue for storage. Why? because use or storage are the only options (other than excretion)." If you want biochemical details of the regulation then your question is too broad to be answered here. You need to read an account of fat metabolism in a biochemistry text book. $\endgroup$
    – David
    May 22, 2016 at 16:09
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    $\begingroup$ I don't think your premise is correct. Acetyl-CoA is not produced at all unless needed, because there is a limited pool of Coenzyme A, which limits Acetyl-CoA abundance. If there is an excess of fat, it is not catabolized to acetyl-CoA at all, but simply stored away until needed. Adipose tissue is capable of taking up fatty acids directly and esterifying them into triacylglycerides (fat). $\endgroup$
    – Roland
    Jun 8, 2016 at 18:06

1 Answer 1


As Roland mentioned in the comments, in the well fed state, not all of the Acyl coA is converted to Acetyl coA. This picture from Harper's Biochemistry, 29th, should come handy. enter image description here

It is the CPT-1 gateway that regulates the amount of acyl-coA (from FFA) that enters into the mitochondria to form acetyl-coA.

In the Fed state, the CPT gateway is shutdown (regulation by malonyl-CoA) - allowing esterification by sending them back as VLDLs. In the starved state, the gates open, leading to beta oxidation giving acetyl-CoA.

The acetyl coA then can enter the Kreb's cycle to get completely oxidised and give ATP + CO2 (this ATP the liver readily utilises). Or, the acetyl-CoA can be channeled into ketogenesis, where this energy can be used by other tissues (since liver lacks the enzyme thiolase and hence can't metabolise ketone bodies). How the liver distributes the acetyl-coA for ketogenesis/Kreb's cycle is a different story altogether.


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