par Fery, Françoise ;D'Attellis, N.P.;Balasse, Edmond
Référence The American journal of physiology, 259, 6 22-6, page (E770-E777)
Publication Publié, 1990
Article révisé par les pairs
Résumé : To analyze the mechanisms of fasting induced glucose intolerance, glucose metabolism was studied before and after the ingestion of 75 g glucose in 24 normal subjects fasted for either 14 h (n = 12) or 4 days (n = 12). The techniques included intravenous infusion of [6-3H] glucose and oral administration of [1-14C] glucose combined with indirect calorimetry. Compared with the controls, the starved subjects exhibited the following differences in glucose metabolism during the 5 h after glucose ingestion. 1) Mean incremental levels were fourfold higher for glucose and 40% higher for insulin. 2) Absorption of oral glucose was delayed and prolonged, but total amount reaching systemic circulation in 5 h was identical in the two groups (~63 g). 3) Suppression of hepatic glucose output was reduced (-12 ± 1 vs. -22 ± 2 g). 4) Consequently, the increment in peripheral appearance of total glucose (exogenous plus endogenous) was augmented (+52 ± 2 vs. +41 ± 2 g). 5) Mean glucose clearance increased significantly less (+28 ± 7 vs. +96 ± 10 ml/min). 6) Oxidation of oral glucose was reduced (9 ± 2 vs. 36 ± 3 g), and nonoxidative disposal (presumably storage) was enhanced (56 ± 2 vs. 36 ± 3 g) in the presence of an elevated fat oxidation (35 ± 2 vs. 22 ± 4 g). Thus the alterations in glucose homeostasis responsible for the starvation-induced glucose intolerance are located both at the splanchnic (hepatic) and peripheral levels.