GLP-1 (glucagon-like peptide-1) is secreted by intestinal L-cells in response to a meal. Its physiological effects relevant to glucose homeostasis include all EXCEPT:

• A Stimulation of glucose-dependent insulin secretion from pancreatic beta cells
• B Inhibition of glucagon secretion from alpha cells (glucose-dependent)
• C Slowing of gastric emptying (incretin effect on gut motility reducing glucose absorption rate)
• D Stimulation of hepatic gluconeogenesis to provide sustained glucose supply post-meal ✓

Explanation

GLP-1 (an incretin hormone) has multiple glucose-lowering actions: (1) Potentiates glucose-stimulated insulin secretion from beta cells via GLP-1R → Gs → cAMP → PKA → enhanced Ca2+ signaling and insulin exocytosis (critically, this effect is glucose-dependent—no hypoglycemia risk at low glucose); (2) Suppresses glucagon from alpha cells in a glucose-dependent manner; (3) Slows gastric emptying, blunting post-meal glucose excursion; (4) Reduces appetite via hypothalamic GLP-1R signaling; (5) May promote beta cell proliferation and reduce apoptosis. Hepatic gluconeogenesis is NOT stimulated by GLP-1—this would oppose its glucose-lowering function. GLP-1 actually reduces glucagon (the main stimulus for gluconeogenesis). GLP-1 receptor agonists (liraglutide, semaglutide) exploit these mechanisms therapeutically.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

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