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Acute effects of pharmacological modifications of fatty acid metabolism on human satiety

Gatta, Blandine ; Zuberbuehler, Christine ; Arnold, Myrtha ; Aubert, Roberte ; Langhans, Wolfgang ; Chapelot, Didier

In: British Journal of Nutrition, 2008, vol. 101, no. 12, p. 1867-1877

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    Titre
    • Acute effects of pharmacological modifications of fatty acid metabolism on human satiety
    Auteur
    • Gatta, Blandine. Service d'Endocrinologie et Maladies Métaboliques, Hôpital du Haut Lévêque, Pessac, 33604, France
    • Zuberbuehler, Christine. Physiology and Behaviour Group, Institute of Animal Sciences, ETH Zurich, Schorerstrasse 16, 8603 Schwerzerbach, Switzerland
    • Arnold, Myrtha. Physiology and Behaviour Group, Institute of Animal Sciences, ETH Zurich, Schorerstrasse 16, 8603 Schwerzerbach, Switzerland
    • Aubert, Roberte. Université Paris 7, INSERM U695, Faculté Xavier Bichat, 75018 Paris, France
    • Langhans, Wolfgang. Physiology and Behaviour Group, Institute of Animal Sciences, ETH Zurich, Schorerstrasse 16, 8603 Schwerzerbach, Switzerland
    • Chapelot, Didier. Université Paris 13, Réponses Cellulaires et Fonctionnelles à l'Hypoxie, EA 2363, UFR Santé Médecine et Biologie Humaine, 93017 Bobigny Cedex, France
    Type de document
    • Postprint
    Langue
    • Inglese
    Publié dans
    • British Journal of Nutrition, 2008, vol. 101, no. 12, p. 1867-1877. Cambridge University Press
    Autre version électronique
    Identifiant OAI-PMH
    • oai:doc.rero.ch:292540
    Summary
    The role of NEFA in eating behaviour is still poorly known. Our objective was to examine whether etomoxir (ETO), an inhibitor of NEFA oxidation, or (−)-hydroxycitrate (HCA), an inhibitor of lipogenesis which may indirectly stimulate NEFA oxidation, alters satiety. Post-lunch satiety was measured in eight normal-weight male subjects who were deprived of time cues and received on three occasions either ETO (320mg), HCA (2g) or placebo (PLA) in random order. Between lunch and dinner, blood was withdrawn continuously and collected every 10min for measures of plasma concentrations of glucose, insulin, lactate, TAG, NEFA, β-hydroxybutyrate (BHB), leptin and ghrelin. Results showed that HCA began to decrease hunger and desire to eat compared to PLA and ETO 210min after lunch and increased satiety duration compared to PLA by 70 (se 23) min (P<0·05), but did not modify energy intake at dinner. ETO did not affect any variable of satiety. HCA increased NEFA concentrations during the pre-dinner period, whereas ETO increased and decreased plasma concentrations of NEFA and BHB, respectively. Mean differences in plasma NEFA concentrations between HCA and PLA were predictive of the differences in satiety duration between treatments (r2 0·71, P<0·01). Among treatments, plasma leptin concentration at dinner onset was the only blood variable correlated with energy intake at this meal (r −0·75, P<0·0005). In healthy, normal-weight men, acute HCA increased the intensity and duration of satiety possibly via increased NEFA disposal for oxidation