Incretin.

Gut hormones (GLP-1, GIP) that boost insulin after eating.

Incretins are gut-derived hormones, chiefly GLP-1 and GIP, released in response to nutrients in the intestine that amplify glucose-dependent insulin secretion. The idea comes from the incretin effect, a long-standing observation that glucose taken by mouth triggers a substantially larger insulin response than the same amount of glucose delivered intravenously. The gut evidently signals the pancreas that food is arriving, ahead of and in addition to the glucose signal itself, and incretins are the messengers doing that. The word matters here because it names the whole category that the modern metabolic drug class is built on. Every GLP-1 receptor agonist, every dual GLP-1 and GIP agonist, and the DPP-4 inhibitors that work by preventing incretin breakdown are all interventions on the incretin system, approached from different angles. The glucose-dependent part of the definition is the clinically important detail: incretin signalling amplifies insulin release when glucose is high and largely stands down when it is not, which is why this mechanism behaves differently from drugs that force insulin release regardless of glucose. The clarification worth making is that incretin is a functional category, not a single molecule, and compounds within it differ substantially in receptor targets and duration.