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Lipid metabolism: malonyl-CoA… MCQ (B7-BIO5-18)

Q: What is the answer to this Biochemistry question?

The best answer is B, Insulin activates acetyl-CoA carboxylase by dephosphorylation, and malonyl-CoA then inhibits CPT-I. In the fed state, insulin promotes dephosphorylation and thus activation of acetyl-CoA carboxylase, raising malonyl-CoA.

Q: What concept does this question test?

It tests Lipid metabolism: malonyl-CoA regulation of oxidation in Biochemistry. Malonyl-CoA is a potent inhibitor of CPT-I at the outer mitochondrial membrane, so newly synthesised fatty acids are not oxidised in a futile cycle and are esterified to triglyceride. In fasting, glucagon and AMPK phosphorylate ACC, lower malonyl-CoA and release CPT-I.

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Biochemistry · Lipid metabolism: malonyl-CoA regulation of oxidation

Sample item

After a carbohydrate-rich meal, hepatic fatty acid oxidation is suppressed even though fatty acids still reach the liver. Which sequence best explains this?

AInsulin activates AMP-activated kinase, which phosphorylates acetyl-CoA carboxylase and raises malonyl-CoABInsulin activates acetyl-CoA carboxylase by dephosphorylation, and malonyl-CoA then inhibits CPT-ICMalonyl-CoA inhibits the acyl-CoA dehydrogenases directly within the mitochondrial matrixDInsulin phosphorylates carnitine palmitoyltransferase II and so inactivates the enzyme

Original practice item, not a recalled exam question. Nothing here is recorded.

The answer and the reasoning

B. Insulin activates acetyl-CoA carboxylase by dephosphorylation, and malonyl-CoA then inhibits CPT-I

In the fed state, insulin promotes dephosphorylation and thus activation of acetyl-CoA carboxylase, raising malonyl-CoA. Malonyl-CoA is a potent inhibitor of CPT-I at the outer mitochondrial membrane, so newly synthesised fatty acids are not oxidised in a futile cycle and are esterified to triglyceride. In fasting, glucagon and AMPK phosphorylate ACC, lower malonyl-CoA and release CPT-I.

Option by option

A. Insulin activates AMP-activated kinase, which phosphorylates acetyl-CoA carboxylase and raises malonyl-CoA
AMPK is activated by energy depletion and phosphorylation of ACC lowers its activity, which would favour oxidation.
B. Insulin activates acetyl-CoA carboxylase by dephosphorylation, and malonyl-CoA then inhibits CPT-I (correct)
Insulin-driven ACC activation raises malonyl-CoA, which blocks CPT-I and the entry of fatty acids to mitochondria.
C. Malonyl-CoA inhibits the acyl-CoA dehydrogenases directly within the mitochondrial matrix
Malonyl-CoA acts on CPT-I at the outer membrane, not on acyl-CoA dehydrogenase.
D. Insulin phosphorylates carnitine palmitoyltransferase II and so inactivates the enzyme
CPT-II sits on the inner membrane and is not the regulated step; insulin does not inactivate it by phosphorylation.

Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.

Lipid metabolism: malonyl-CoA regulation of oxidation: practice question

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The answer and the reasoning

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