Incretin

Deep dive

Incretin: complete reference

An incretin is a gut-derived hormone that increases insulin secretion from the pancreas in response to food intake, accounting for what is called the “incretin effect” — the observation that oral glucose produces a larger insulin response than equivalent intravenous glucose. The two principal human incretins are GLP-1 (secreted by intestinal L-cells) and GIP (secreted by intestinal K-cells). The incretin effect is responsible for approximately 50-70% of postprandial insulin secretion in healthy individuals but is dramatically reduced in patients with type 2 diabetes — leading to the “incretin deficiency” that pharmaceutical GLP-1 receptor agonists and DPP-4 inhibitors are designed to address. Beyond insulin secretion, incretins also affect glucagon release, gastric emptying, and appetite regulation through receptors expressed in pancreatic islets, gastrointestinal tract, and central nervous system. The incretin axis has become one of the most therapeutically targeted pathways in metabolic medicine.

In practice

When you eat a bowl of rice, your gut releases incretins (GLP-1 and GIP) that signal your pancreas to release insulin before the glucose hits your bloodstream — preventing a sugar spike.

Clinical context

The therapeutic strategies targeting incretins are: GLP-1 receptor agonists (replace deficient signaling), DPP-4 inhibitors (prevent native incretin degradation), and dual GIP/GLP-1 agonists (target both receptors).