Incretin

Incretins are the gut’s “food just arrived” hormones. When you eat, cells in your intestine release these hormones, and their main message to the pancreas is: get ready, release insulin. They’re the reason a meal you eat triggers more insulin than the same amount of sugar delivered straight into a vein — your gut is actively signaling ahead, not just reacting to blood sugar.

There are two main ones: GLP-1 and GIP (glucose-dependent insulinotropic polypeptide). Both nudge insulin after eating; GLP-1 also curbs appetite and slows the stomach. A nice feature is that they work in a glucose-dependent way — they mainly push insulin when blood sugar is actually up, which makes them less likely to crash it too low.

This is the family behind the newest wave of diabetes and weight-loss drugs. Semaglutide copies GLP-1. Tirzepatide goes further and mimics both GLP-1 and GIP at once — a “dual incretin” — which is part of why it tends to outperform GLP-1-only drugs on weight.

For a concrete example, semaglutide is a GLP-1 receptor agonist: it copies one arm of the incretin system rather than supplying insulin itself. Tirzepatide is a dual agonist that activates receptors for both GLP-1 and GIP, so it shows why “incretin drug” can mean more than a GLP-1-only compound. In both cases, the drug acts at receptors used by normal post-meal signals, but it is engineered to keep that receptor message going much longer than the natural hormone would. That is the practical distinction when reading a medication page: incretins are the body’s short-lived signals; these compounds are longer-acting drugs built around those signals.

So when you see “incretin” in coverage of these medications, read it as the umbrella term: the class of gut hormones being imitated. GLP-1 is the famous member; incretin is the family it belongs to.