Current developments in nutrition · 2026
Specific Collagen Peptides Support Postprandial Metabolic Health by Modulating Incretin Hormones, Gastric Transit, and Glycemic Control in Participants with Normoglycemia and Prediabetes.
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Virgilio Nicolina, Schön Christiane, Steiner Nicole, Schlageter Vincent, Wilhelm Manfred, Silva Catarina If, Gevaert Elien, Prawitt Janne
Аннотация
BACKGROUND: Nutritional preload strategies can improve postprandial glycemic control through modulation of incretin secretion. We previously identified specific collagen peptides (CP; Nextida GC) that stimulate glucagon-like peptide-1 (GLP-1) secretion in vitro and improve postprandial glycemic responses in preclinical models and a pilot human study.
OBJECTIVES: This study aims to investigate the effects of a CP preload on postprandial glycemic control and to characterize the associated hormonal and physiological responses in participants with normoglycemia or prediabetes.
METHODS: In a randomized, double-blind, placebo-controlled, crossover study, 30 participants (12 normoglycemic and 18 prediabetic) ingested 10 g CP or placebo 30 min before a standardized carbohydrate-rich meal (preload phase). Plasma glucose, serum insulin, C-peptide, GLP-1, and glucose-dependent insulinotropic polypeptide (GIP) concentrations were measured during the preload and postprandial periods. As a potential physiological mechanism, gastric transit was assessed via the gastric residence time of an indigestible capsule.
RESULTS: During the preload phase, CP significantly increased insulin and incretin levels (GLP-1 and GIP) compared with placebo (all P < 0.0001). After the meal, CP significantly reduced postprandial glucose excursions (incremental area under the curve (iAUC)0-180 min, P = 0.0178), whereas total insulin responses were unchanged (iAUC-30-180 min, P = 0.8929). Furthermore, CP prolonged the gastric residence time of the indigestible 3D-Transit capsule in the prediabetic subgroup (P = 0.0436).
CONCLUSIONS: A 10 g preload of CP improved postprandial glycemic control without increasing overall postprandial insulin exposure. These effects were accompanied by early stimulation of insulin and incretin hormones and, in individuals with prediabetes, prolonged gastric residence time. The findings suggest that CP may support healthy postprandial metabolic regulation through complementary hormonal and physiological mechanisms.This study was registered at clinicaltrials.gov as NCT06789263.
OBJECTIVES: This study aims to investigate the effects of a CP preload on postprandial glycemic control and to characterize the associated hormonal and physiological responses in participants with normoglycemia or prediabetes.
METHODS: In a randomized, double-blind, placebo-controlled, crossover study, 30 participants (12 normoglycemic and 18 prediabetic) ingested 10 g CP or placebo 30 min before a standardized carbohydrate-rich meal (preload phase). Plasma glucose, serum insulin, C-peptide, GLP-1, and glucose-dependent insulinotropic polypeptide (GIP) concentrations were measured during the preload and postprandial periods. As a potential physiological mechanism, gastric transit was assessed via the gastric residence time of an indigestible capsule.
RESULTS: During the preload phase, CP significantly increased insulin and incretin levels (GLP-1 and GIP) compared with placebo (all P < 0.0001). After the meal, CP significantly reduced postprandial glucose excursions (incremental area under the curve (iAUC)0-180 min, P = 0.0178), whereas total insulin responses were unchanged (iAUC-30-180 min, P = 0.8929). Furthermore, CP prolonged the gastric residence time of the indigestible 3D-Transit capsule in the prediabetic subgroup (P = 0.0436).
CONCLUSIONS: A 10 g preload of CP improved postprandial glycemic control without increasing overall postprandial insulin exposure. These effects were accompanied by early stimulation of insulin and incretin hormones and, in individuals with prediabetes, prolonged gastric residence time. The findings suggest that CP may support healthy postprandial metabolic regulation through complementary hormonal and physiological mechanisms.This study was registered at clinicaltrials.gov as NCT06789263.