Nucleotide metabolism: fructose and hyperuricaemia: 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 · Nucleotide metabolism: fructose and hyperuricaemia

Sample item

A man with obesity drinks large quantities of fructose-sweetened beverages daily and has a raised serum urate and recurrent gout. Which mechanism links heavy fructose intake to urate production?

ARapid hepatic phosphorylation of fructose consumes ATP, and the AMP formed is degraded to uric acidBFructose directly inhibits xanthine oxidase in the liverCFructose is converted to PRPP in the pentose phosphate pathwayDFructose is converted directly to uric acid by fructokinase

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

The answer and the reasoning

A. Rapid hepatic phosphorylation of fructose consumes ATP, and the AMP formed is degraded to uric acid

Fructokinase phosphorylates fructose rapidly and without feedback control, rapidly consuming ATP and releasing AMP. AMP is deaminated to IMP and then catabolised through hypoxanthine and xanthine to uric acid. The same mechanism explains hyperuricaemia after fructose loading in hereditary fructose intolerance.

Option by option

A. Rapid hepatic phosphorylation of fructose consumes ATP, and the AMP formed is degraded to uric acid (correct)
Correct. ATP depletion drives AMP breakdown and urate formation.
B. Fructose directly inhibits xanthine oxidase in the liver
Fructose does not inhibit xanthine oxidase; inhibition would lower urate.
C. Fructose is converted to PRPP in the pentose phosphate pathway
Fructose is not a precursor of PRPP in this way, and the pentose phosphate pathway is regulated by NADPH need.
D. Fructose is converted directly to uric acid by fructokinase
Fructokinase phosphorylates fructose and does not form uric acid from it directly.

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.

Questions about this Biochemistry question

What is the answer to this Biochemistry question?

The best answer is A, Rapid hepatic phosphorylation of fructose consumes ATP, and the AMP formed is degraded to uric acid. Fructokinase phosphorylates fructose rapidly and without feedback control, rapidly consuming ATP and releasing AMP.

Why is "Fructose directly inhibits xanthine oxidase in the liver" not the answer?

Fructose does not inhibit xanthine oxidase; inhibition would lower urate.

Why is "Fructose is converted to PRPP in the pentose phosphate pathway" not the answer?

Fructose is not a precursor of PRPP in this way, and the pentose phosphate pathway is regulated by NADPH need.

Why is "Fructose is converted directly to uric acid by fructokinase" not the answer?

Fructokinase phosphorylates fructose and does not form uric acid from it directly.

What concept does this question test?

It tests Nucleotide metabolism: fructose and hyperuricaemia in Biochemistry. AMP is deaminated to IMP and then catabolised through hypoxanthine and xanthine to uric acid. The same mechanism explains hyperuricaemia after fructose loading in hereditary fructose intolerance.

How hard is this question?

We tag it as a multi-step question: it asks you to combine more than one idea. 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 Nucleotide metabolism: fructose and hyperuricaemia?

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.