The pharmacological or nutritional intervention targeting the incretin axis, a gut-brain signaling system that regulates glucose-dependent insulin secretion, gastric emptying, and appetite control. Manipulation involves using agents, such as GLP-1 receptor agonists, to enhance the activity of endogenous incretin hormones like Glucagon-like peptide-1 (GLP-1) and Glucose-dependent insulinotropic polypeptide (GIP). This is a primary strategy in modern metabolic medicine for managing blood glucose and promoting sustained weight loss.
Origin
The pathway’s clinical relevance began with the discovery of incretin hormones in the mid-20th century and the subsequent understanding of the “incretin effect,” which is the observation that oral glucose elicits a greater insulin response than intravenous glucose. The development of stable, long-acting synthetic incretin analogues in the early 21st century revolutionized the treatment of type 2 diabetes and obesity. The term highlights the deliberate clinical leveraging of this intrinsic entero-endocrine signaling loop.
Mechanism
Incretin-based agents bind to and activate the GLP-1 and/or GIP receptors on pancreatic beta cells, potentiating glucose-stimulated insulin release in a concentration-dependent manner, thereby lowering postprandial blood sugar. Simultaneously, these signals travel to the brain’s satiety centers and slow gastric motility, promoting a feeling of fullness and reducing caloric intake. This dual action provides powerful metabolic regulation and facilitates sustained changes in body composition and energy homeostasis.
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