GI physiology: incretins: practice question

A Physiology 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.

Try it

Physiology · GI physiology: incretins

Sample item

In a healthy volunteer, an oral glucose load produces a much larger insulin response than an intravenous glucose infusion that gives the same plasma glucose curve. What explains this difference?

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

The answer and the reasoning

A. Release of GLP-1 and GIP from the gut, which amplify glucose-dependent insulin secretion

The incretin effect is the greater insulin response to oral than to intravenous glucose. GLP-1 from intestinal L cells and GIP from K cells potentiate insulin secretion in a glucose-dependent manner and GLP-1 also suppresses glucagon. They are rapidly degraded by DPP-4, which is why DPP-4 inhibitors and GLP-1 receptor agonists are used in type 2 diabetes.

Option by option

  • A. Release of GLP-1 and GIP from the gut, which amplify glucose-dependent insulin secretion (correct)

    Incretin hormones from the gut account for the extra insulin response.

  • B. Release of glucagon from the intestine

    Intestinal glucagon is not the mediator; incretins suppress glucagon in a glucose-dependent way.

  • C. Greater hepatic uptake of glucose after oral administration

    Hepatic uptake does not alter the plasma glucose curve matched between conditions.

  • D. Direct stimulation of beta cells by glucose in the portal vein only

    Beta cells respond to glucose in the systemic circulation equally, so a portal effect does not explain the gap.

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.

More Physiology questions

Questions about this Physiology question

What is the answer to this Physiology question?

The best answer is A, Release of GLP-1 and GIP from the gut, which amplify glucose-dependent insulin secretion. The incretin effect is the greater insulin response to oral than to intravenous glucose.

Why is "Release of glucagon from the intestine" not the answer?

Intestinal glucagon is not the mediator; incretins suppress glucagon in a glucose-dependent way.

Why is "Greater hepatic uptake of glucose after oral administration" not the answer?

Hepatic uptake does not alter the plasma glucose curve matched between conditions.

Why is "Direct stimulation of beta cells by glucose in the portal vein only" not the answer?

Beta cells respond to glucose in the systemic circulation equally, so a portal effect does not explain the gap.

What concept does this question test?

It tests GI physiology: incretins in Physiology. GLP-1 from intestinal L cells and GIP from K cells potentiate insulin secretion in a glucose-dependent manner and GLP-1 also suppresses glucagon. They are rapidly degraded by DPP-4, which is why DPP-4 inhibitors and GLP-1 receptor agonists are used in type 2 diabetes.

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 GI physiology: incretins?

For each system, sketch the key graph (pressure–volume loop, oxygen dissociation curve, nephron handling) and explain it aloud. Then use the flashcards and the other Physiology 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.