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Am J Clin Nutr 90: 1236-1243, 2009. First published September 23, 2009; doi:10.3945/ajcn.2009.28095
American Journal of Clinical Nutrition, doi:10.3945/ajcn.2009.28095
Vol. 90, No. 5, 1236-1243, November 2009

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© 2009 American Society for Clinical Nutrition

ORIGINAL RESEARCH COMMUNICATION

Gut microbiota fermentation of prebiotics increases satietogenic and incretin gut peptide production with consequences for appetite sensation and glucose response after a meal1,2,3

Patrice D Cani, Elodie Lecourt, Evelyne M Dewulf, Florence M Sohet, Barbara D Pachikian, Damien Naslain, Fabienne De Backer, Audrey M Neyrinck and Nathalie M Delzenne

1 From the Louvain Drug Research Institute, Metabolism and Nutrition Research Group, Université Catholique de Louvain, Brussels, Belgium.

2 NMD and PDC are recipients of Fonds speciaux de recherches and Fonds de la recherche scientifique medicale grants (Université Catholique de Louvain, Brussels, Belgium). Financial support has been provided by grants from the Walloon Region (General Directory of Agriculture) and FRS-FNRS (Fonds de la Recherche Scientifique) no. 1.5.095.09.F.

3 Address correspondence to PD Cani or NM Delzenne, UCL, Unit PMNT-7369, Avenue E Mounier, 73/69, B-1200 Brussels, Belgium. E-mail: patrice.cani{at}uclouvain.be or nathalie.delzenne{at}uclouvain.be.

Background: We have previously shown that gut microbial fermentation of prebiotics promotes satiety and lowers hunger and energy intake in humans. In rodents, these effects are associated with an increase in plasma gut peptide concentrations, which are involved in appetite regulation and glucose homeostasis.

Objective: Our aim was to examine the effects of prebiotic supplementation on satiety and related hormones during a test meal for human volunteers by using a noninvasive micromethod for blood sampling to measure plasma gut peptide concentrations.

Design: This study was a randomized, double-blind, parallel, placebo-controlled trial. A total of 10 healthy adults (5 men and 5 women) were randomly assigned to groups that received either 16 g prebiotics/d or 16 g dextrin maltose/d for 2 wk. Meal tolerance tests were performed in the morning to measure the following: hydrogen breath test, satiety, glucose homeostasis, and related hormone response.

Results: We show that the prebiotic treatment increased breath-hydrogen excretion (a marker of gut microbiota fermentation) by {approx}3-fold and lowered hunger rates. Prebiotics increased plasma glucagon-like peptide 1 and peptide YY concentrations, whereas postprandial plasma glucose responses decreased after the standardized meal. The areas under the curve for plasma glucagon-like peptide 1 and breath-hydrogen excretion measured after the meal (0–60 min) were significantly correlated (r = 0.85, P = 0.007). The glucose response was inversely correlated with the breath-hydrogen excretion areas under the curve (0–180 min; r = –0.73, P = 0.02).

Conclusion: Prebiotic supplementation was associated with an increase in plasma gut peptide concentrations (glucagon-like peptide 1 and peptide YY), which may contribute in part to changes in appetite sensation and glucose excursion responses after a meal in healthy subjects.







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