What is the Origin of Incretin Effect?

The concept originated in the early 20th century from observations that oral glucose administration resulted in a more potent insulin release than intravenous administration, suggesting a humoral factor from the gut was involved. The term "incretin" was coined in the 1930s, combining intestine and secretion, but the effect was only precisely characterized in the 1960s and 70s with the discovery and functional identification of the key peptide hormones, GIP and GLP-1.

What is the Mechanism of Incretin Effect?

The mechanism is initiated by the rapid release of incretin hormones from enteroendocrine cells in the small intestine upon nutrient detection. These peptides travel via the circulation to the pancreatic beta-cells, where they bind to specific G-protein coupled receptors. This binding activates intracellular signaling pathways, notably increasing cyclic AMP (cAMP), which potentiates the glucose-stimulated release of insulin. This dual-signal system—glucose plus incretin—ensures that insulin secretion is proportional to the meal size and occurs promptly to manage the incoming nutrient load.

Incretin Effect

Meaning

The Incretin Effect is the physiological phenomenon where the insulin secretory response to orally ingested glucose is significantly greater than the insulin response elicited by an equivalent amount of glucose administered intravenously. This augmented secretion is mediated by a class of gastrointestinal hormones, primarily Glucagon-Like Peptide-1 (GLP-1) and Glucose-dependent Insulinotropic Polypeptide (GIP), which are released from the gut in response to nutrient ingestion. A diminished incretin effect is a characteristic metabolic defect observed in patients with Type 2 Diabetes Mellitus.

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