Splanchnic tissues play a crucial role in uremic glucose intolerance
Résumé
Objective: Determine the mechanism of glucose intolerance in chronically uremic subjects. Design: Comparison of doubly labeled oral glucose tolerance tests. Subjects: Seven nondialyzed chronically uremic subjects (creatinine, 420 ± 104 μmol/L) and 7 healthy subjects, matched for age and body mass index. Intervention: Plasma glucose was labeled by an infusion of dideuterated glucose started 120 minutes before ingestion of 1 g/kg of naturally 13C-enriched corn starch glucose. Glucose levels and oxidation were monitored for 330 minutes after glucose ingestion. Results: Uremic subjects had normal fasting plasma glucose levels and impaired glucose tolerance with high plasma insulin (P < .001 versus controls). Glucose tolerance was impaired because of an increased total rate of appearance of glucose (cumulated on 330 minutes: uremic, 1,231 ± 42 mg/kg/330 min, controls, 1,031 ± 64; P < .05). Peripheral glucose uptake was increased (P < .05) because of an increased nonoxidative disposal (P = .051). Conclusions: Although peripheral glucose uptake resisted the stimulatory effect of the high insulin levels, glucose tolerance was impaired through splanchnic metabolic disturbances: reduced splanchnic glucose uptake and increased endogenous glucose production. The respective contribution of these abnormalities remains to be determined.