Effects of dexamethasone on hepatic glucose production and fructose
metabolism in healthy humans.
Tounian, P., P. Schneiter, S. Henry, J. Delarue, and L. tappy.
Institute of Physiology, Faculty of Medicine, University of
Lausanne, 1005 Lausanne, Switzerland
APStracts 4:0095E, 1997.
This study was designed to determine whether glucocorticoids alter
autoregulation of glucose production and fructose metabolism. Two
protocols with either dexamethasone (DEX) or placebo (PLACEBO) were
performed in six healthy men during hourly ingestion of [13C]fructose
(1.33 mmol.kg 1.h 1) for 3h. In both protocols, endogenous glucose
production (EGP) increased by 8% (PLACEBO) and 7% (DEX) after
fructose, whereas gluconeogenesis from fructose represented 82%
(PLACEBO) and 72% (DEX) of EGP. Fructose oxidation measured from
breath 13CO2 was similar in both protocols (9.3 0.7 (PLACEBO) and 9.6
0.5 mol.kg 1.min 1 (DEX)). Non oxidative carbohydrate disposal,
calculated as fructose administration rate minus net carbohydrate
oxidation rate after fructose ingestion measured by indirect
calorimetry, was also similar in both protocols (5.8 0.8 (PLACEBO)
and 5.9 2.0 mol.kg1.min1 (DEX)). It is concluded that dexamethasone
1) does not alter the autoregulatory process that prevents a
fructose-induced increase in gluconeogenesis from increasing total
glucose production, and 2)does not affect oxidative and non oxidative
pathways of fructose. This indicates that the insulin-regulated
enzymes involved in these pathways are not affected in a major way by
dexamethasone.
Received 3 October 1996; accepted in final form 27 March 1997.
APS Manuscript Number E541-6.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 13 May 1997