Normalization of carbohydrate-induced thermogenesis by fructose in insulin-resistant states

Détails

ID Serval
serval:BIB_1CDADE21ADC1
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Normalization of carbohydrate-induced thermogenesis by fructose in insulin-resistant states
Périodique
American Journal of Physiology
Auteur⸱e⸱s
Simonson  D. C., Tappy  L., Jequier  E., Felber  J. P., DeFronzo  R. A.
ISSN
0002-9513 (Print)
Statut éditorial
Publié
Date de publication
02/1988
Volume
254
Numéro
2 Pt 1
Pages
E201-7
Notes
Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S. --- Old month value: Feb
Résumé
To examine whether defects in carbohydrate oxidation and thermogenesis in aging, obesity, and diabetes are secondary to impaired insulin action or to a primary defect in intracellular metabolism, we compared substrate oxidation and energy expenditure in 9 younger, 9 older, 9 obese, and 10 non-insulin-dependent diabetic subjects after the ingestion of 75 g of glucose or fructose (a monosaccharide whose transport into the cell and subsequent metabolism are independent of insulin). In young control subjects fructose produced a significantly greater increase in carbohydrate oxidation and energy expenditure than glucose despite significantly lower plasma glucose and insulin levels. In aged, obese, and diabetic individuals the increments in carbohydrate oxidation and energy expenditure after glucose ingestion were significantly imparied versus the younger controls. After fructose ingestion the increase in carbohydrate oxidation in the three insulin-resistant groups remained below that observed in the younger volunteers, whereas carbohydrate-induced thermogenesis was enhanced to levels that were comparable with those seen in the younger group. These data suggest that 1) the stimulation of thermogenesis after fructose ingestion is related to an augmentation of intracellular metabolism rather than an increase in the plasma insulin concentration per se, 2) the insulin resistance of aging, obesity, and diabetes is associated with a defect in intracellular carbohydrate oxidation, and 3) the cellular mechanisms involved in carbohydrate-induced thermogenesis are not primarily impaired in insulin-resistant states.
Mots-clé
Blood Glucose/analysis Body Temperature Regulation/*drug effects Carbohydrates/*pharmacology Diabetes Mellitus, Type 2/metabolism/physiopathology Energy Metabolism Fatty Acids, Nonesterified/blood Fructose/blood/*pharmacology Humans Insulin/blood *Insulin Resistance Obesity/metabolism/physiopathology Oxidation-Reduction Reference Values
Pubmed
Web of science
Création de la notice
24/01/2008 13:36
Dernière modification de la notice
20/08/2019 12:53
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