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Associations between postprandial insulin and blood glucose responses, appetite sensations and energy intake in normal weight and overweight individuals: a meta-analysis of test meal studies

Journal

BRITISH JOURNAL OF NUTRITION
Volume 98, Issue 1, Pages 17-25

Publisher

CAMBRIDGE UNIV PRESS
DOI: 10.1017/S000711450768297X

Keywords

insulin; glucose; short-term appetite regulation; energy intake; overweight

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is unclear whether postprandial blood glucose or insulin exerts a regulatory function in short-term appetite regulation in humans. The aim of this study was to investigate, by use of meta-analysis, the role of blood glucose and insulin in short-term appetite sensation and energy intake (EI) in normal weight and overweight participants. Data from seven test meal studies were used, including 136 healthy participants (ALL) (92 normal weight (NW) and 44 overweight or obese (OW)). All meals were served as breakfasts after an overnight fast, and appetite sensations and blood samples were obtained frequently in the postprandial period. Finally, an ad libitum lunch was served. Data were analysed by fixed effects study level (SL) meta-regression analysis and individual participant data (IPD) regression analysis, using STATA software. In SL analysis, postprandial insulin response was associated with decreased hunger in ALL, NW and OW (P< 0 center dot 0 19), and with increased satiety in NW (P= 0.004) and lower subsequent El in OW (P=0 center dot 022). Multivariate IPD analysis showed similar associations, but only in NW for hunger, satiety and El (P < 0.028), and in ALL for El (P=0 center dot 016). The only association involving blood glucose was the multivariate IPD analysis showing an inverse association between blood glucose and El in ALL (P=0 center dot 032). Our results suggest that insulin, but not glucose, is associated with short-term appetite regulation in healthy participants, but the relationship is disrupted in the overweight and obese. We conclude that the postprandial insulin response may be an important satiety signal, and that central nervous system insulin resistance in overweight might explain the blunted effect on appetite.

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