Hepatic insulin resistance in obese non-diabetic subjects and in type 2 diabetic patients

Détails

ID Serval
serval:BIB_F0940BBC663C
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Hepatic insulin resistance in obese non-diabetic subjects and in type 2 diabetic patients
Périodique
Obesity Research
Auteur(s)
Paquot  N., Scheen  A. J., Dirlewanger  M., Lefebvre  P. J., Tappy  L.
ISSN
1071-7323 (Print)
Statut éditorial
Publié
Date de publication
03/2002
Volume
10
Numéro
3
Pages
129-34
Notes
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: Mar
Résumé
OBJECTIVE: Obese non-diabetic patients are characterized by an extra-hepatic insulin resistance. Whether obese patients also have decreased hepatic insulin sensitivity remains controversial. RESEARCH METHODS AND PROCEDURES: To estimate their hepatic insulin sensitivity, we measured the rate of exogenous insulin infusion required to maintain mildly elevated glycemia in obese patients with type 2 diabetes, obese non-diabetic patients, and lean control subjects during constant infusions of somatostatin and physiological low-glucagon replacement infusions. To account for differences in insulin concentrations among the three groups of subjects, an additional protocol was also performed in healthy lean subjects with higher insulin infusion rates and exogenous dextrose infusion. RESULTS: The insulin infusion rate required to maintain glycemia at 8.5 mM was increased 4-fold in obese patients with type 2 diabetes and 1.5-fold in obese non-diabetic patients. The net endogenous glucose production (measured with 6,6-(2)H(2)-glucose) and total glucose output (measured with 2-(2)H(1)-glucose) were approximately 30% lower in the patients than in the lean subjects. Net endogenous glucose production and total glucose output were both markedly increased in both groups of obese patients compared with lean control subjects during hyperinsulinemia. DISCUSSION: Our data indicate that both obese non-diabetic and obese type 2 diabetic patients have a blunted suppressive action of insulin on glucose production, indicating hepatic and renal insulin resistance.
Mots-clé
Adult Aged Blood Glucose/analysis Diabetes Mellitus/*metabolism Diabetes Mellitus, Type 2/*metabolism Fatty Acids, Nonesterified/blood Female Glucagon/blood Humans Insulin/blood/pharmacology Insulin Resistance/*physiology Liver/*physiopathology Male Middle Aged Obesity/*metabolism Somatostatin/pharmacology
Pubmed
Web of science
Création de la notice
24/01/2008 14:36
Dernière modification de la notice
03/03/2018 22:36
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