EFFECTS OF DEXAMETHASONE ON HEPATIC GLUCOSE-PRODUCTION AND FRUCTOSE METABOLISM IN HEALTHY HUMANS

This study was designed to determine whether glucocorticoids alter aut oregulation of glucose production and fructose metabolism. Two protoco ls with either dexamethasone (DEX) or placebo (Placebo) were performed in six healthy men during hourly ingestion of [C-13]fructose (1.33 mm ol.kg(-1).h(-1)) for 3 h. In both protocols, endogenous glucose produc tion (EGP) increased by 8 (Placebo) and 7% (DEX) after fructose, where as gluconeogenesis from fructose represented 82 (Placebo) and 72% (DEX ) of EGP Fructose oxidation measured from breath (CO2)-C-13 was Simila r in both protocols [9.3 +/- 0.7 (Placebo) and 9.6 +/- 0.5 mu mol.kg(- 1).min(-1) (DEX)]. Nonoxidative carbohydrate disposal, calculated as f ructose administration rate minus net carbohydrate oxidation rate afte r fructose ingestion measured by indirect calorimetry, was also simila r in both protocols [5.8 +/- 0.8 (Placebo) and 5.9 +/- 2.0 mu mol.kg(- 1).min(-2) (DEX)]. We concluded that dexamethasone 1) does not alter t he autoregulatory process that prevents a fructose-induced increase in gluconeogenesis from increasing total glucose production and 2) does not affect oxidative and nonoxidative pathways of fructose. This indic ates that the insulin-regulated enzymes involved in these pathways are not affected in a major way by dexamethasone.