Lipid metabolism: fatty liver in kwashiorkor: practice question

A Biochemistry question in the style of the NEET PG paper. Answer it first, then read why the right option is right and why each of the others is wrong.

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Biochemistry · Lipid metabolism: fatty liver in kwashiorkor

Sample item

A 2-year-old on a low-protein, starchy diet has oedema and an enlarged, fatty liver. Which mechanism best explains the hepatic fat accumulation?

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

The answer and the reasoning

C. Inadequate apolipoprotein synthesis impairs VLDL export of triglyceride

Protein deficiency limits synthesis of apoB-100 and other proteins needed to assemble and secrete VLDL, so triglyceride made from dietary carbohydrate and mobilised fatty acids stays in the liver. Lipotropic factors and adequate protein allow fat export.

Option by option

  • A. Failure of lipolysis in adipose tissue

    Adipose lipolysis is increased in malnutrition and supplies fatty acids to the liver, so failure of lipolysis does not occur.

  • B. Excess dietary protein diverted into lipogenesis

    The diet is low in protein, not high, so dietary protein excess cannot be the cause.

  • C. Inadequate apolipoprotein synthesis impairs VLDL export of triglyceride (correct)

    Correct. Too little protein for apoB-100 impairs VLDL assembly and triglyceride export.

  • D. Increased hepatic oxidation of fatty acids

    Increased fatty acid oxidation would lower hepatic fat, not raise it.

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.

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Questions about this Biochemistry question

What is the answer to this Biochemistry question?

The best answer is C, Inadequate apolipoprotein synthesis impairs VLDL export of triglyceride. Protein deficiency limits synthesis of apoB-100 and other proteins needed to assemble and secrete VLDL, so triglyceride made from dietary carbohydrate and mobilised fatty acids stays in the liver.

Why is "Failure of lipolysis in adipose tissue" not the answer?

Adipose lipolysis is increased in malnutrition and supplies fatty acids to the liver, so failure of lipolysis does not occur.

Why is "Excess dietary protein diverted into lipogenesis" not the answer?

The diet is low in protein, not high, so dietary protein excess cannot be the cause.

Why is "Increased hepatic oxidation of fatty acids" not the answer?

Increased fatty acid oxidation would lower hepatic fat, not raise it.

What concept does this question test?

It tests Lipid metabolism: fatty liver in kwashiorkor in Biochemistry. Lipotropic factors and adequate protein allow fat export.

How hard is this question?

We tag it as an application question: it asks you to use a fact on a patient or a finding. The tag is our own editorial judgement, not an official difficulty rating, so read the reason for every option, not only the answer.

How should I study Lipid metabolism: fatty liver in kwashiorkor?

Build one table of enzyme deficiency, disease, inheritance and key finding, then revise it by spaced recall. Then use the flashcards and the other Biochemistry questions on this site to test what stuck.

Is this a real NEET PG question?

No. It is an original practice item (editorial status: sample, version 1). NextPrep does not publish recalled or leaked questions, and independent faculty review of this item has not been completed yet, so confirm important facts in a standard textbook.