Effect of lipid oxidation on glucose utilization in humans.

Détails

ID Serval
serval:BIB_7222
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Synthèse (review): revue aussi complète que possible des connaissances sur un sujet, rédigée à partir de l'analyse exhaustive des travaux publiés.
Collection
Publications
Institution
Titre
Effect of lipid oxidation on glucose utilization in humans.
Périodique
American Journal of Clinical Nutrition
Auteur⸱e⸱s
Jéquier E.
ISSN
0002-9165
Statut éditorial
Publié
Date de publication
1998
Volume
67
Numéro
3 Suppl.
Pages
527S-530S
Langue
anglais
Notes
Publication types: Journal Article ; Review
Résumé
The mechanisms responsible for the competition between glucose and fatty acids as oxidative fuels are not yet completely understood in humans. Maintenance of plasma fatty acid concentrations by means of lipid and heparin infusion during hyperinsulinemic, euglycemic clamps in humans first suppresses glucose oxidation and only later decreases nonoxidative glucose disposal; muscle pyruvate dehydrogenase activity is inhibited when plasma fatty acid concentrations are maintained during hyperinsulinemic, euglycemic clamps. The maintenance of plasma fatty acid concentrations impairs insulin-stimulated muscle glucose uptake only if fatty acid uptake by skeletal muscles is increased. The role of hyperglycemia in glucose-fatty acid competition has recently been emphasized. Fatty acid utilization by muscle is impaired in patients with type 2 diabetes mellitus during fasting hyperglycemia: both lipid oxidation and uptake of plasma fatty acids by skeletal muscle are impaired during postabsorptive conditions. Hyperglycemia indirectly activates pyruvate dehydrogenase, the rate-limiting enzyme for glucose oxidation. The ability of increased glucose availability to stimulate glucose oxidation and reduce lipid oxidation by skeletal muscle can be considered a corollary of the Randle glucose-fatty acid cycle. It can be concluded that within a reasonable range of carbohydrate-to-fat ratios, the addition of fat to a meal does not decrease postprandial carbohydrate oxidation. Furthermore, high-fat meals do not promote fat oxidation leading to fat storage in adipose tissue.
Mots-clé
Diabetes Mellitus, Type 2/blood, Dietary Carbohydrates/metabolism, Dietary Fats/metabolism, Fatty Acids/metabolism, Glucose/metabolism, Humans, Hyperglycemia/metabolism, Insulin/blood, Insulin Resistance, Oxidation-Reduction
Pubmed
Web of science
Création de la notice
19/11/2007 12:45
Dernière modification de la notice
20/08/2019 14:30
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