Disruption of Anticipatory Insulin Secretion in Patients with Hyperglycemia and Obesity

In obesity and pre-diabetes, anticipatory insulin secretion is disrupted: GLP-1 and ISR profiles decline prematurely, prolonging post-prandial hyperglycemia.

• Why it matters: Anticipatory insulin secretion can reduce glycemic excursions, but dysglycemia may impair the beta-cell timing signals needed for future glucose control.
• What they did: In healthy individuals, ISR tracked future blood glucose best over 6+-1 minutes, while GLP-1 shifted by 9+-3 minutes; in obesity and pre-diabetes, these profiles declined early, and semaglutide increased ISR yet abolished anticipatory timing.
• The result: Semaglutide increased ISR and curbed hyperglycemia, but it abolished anticipatory insulin secretion, causing ISR and glucose profiles to overlap and delaying insulin relative to glucose with higher post-prandial glycemic undershoots.

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