Impaired glucose oxidation and glucose-induced thermogenesis in renal transplant recipients

Background. Renal transplant recipients often show various metabolic abnorm alities including reduced glucose tolerance, impaired insulin sensitivity a nd altered lipid metabolism. However, the acute effects of carbohydrate ing estion on substrate utilization and energy expenditure have not been fully elucidated. Methods. We evaluated: (i) basal energy expenditure (EE) and substrate util ization, (ii) metabolic fate of an oral glucose load, and (iii) substrate-i nduced thermogenesis in: (a) 15 non-diabetic renal transplant recipients (T x) (BMI 25 +/- 1) an triple immunosuppressive therapy, (b) 11 patients with primary glomerulonephritis (BMI 25 +/- 1) (Cort) receiving prednisone trea tment, and (c) 12 healthy subjects (BMI 26 +/-1) (N) Continuous indirect ca lorimetry was performed in the basal post-absorptive state for 60 min and c ontinued for an additional 180 min following an oral glucose load (75 g). Results. In the basal state, EE was similar in the three study groups. It a veraged 14.6 +/- 0.7, 15.7 +/- 1.3, and 14.1 +/- 018 cal/kg/min in Tx, Cort , and N respectively. Glucose oxidation was higher in N (1.3 +/- 0.2 mg/kg/ min) than in Tx (0.7 +/- 0.2) and Cort (1.0 +/- 0.2) (P < 0.05 in N vs Tx a nd vs Cort), whereas lipid oxidation was lower in N (0.6 +/- 0.1 mg/kg/min) than in Tx (0.9 +/- 0.1) and Cart (0.9 +/- 0.05) (P < 0.03 in N vs Tx and vs Cort). After glucose ingestion, total carbohydrate oxidation averaged 21 .2 +/- 2, 31.0 +/- 3, and 29.6 +/- 3 g, which represented 28 +/- 3, 41 +/- 3 and 39 +/- 2% of the total glucose load in Tx, Cort and N respectively (P < 0.01 Tx vs Cort and N). The cumulative increase of EE (180 min) was 9.7 +/- 2, 13.2 +/- 3 and 13 +/- 3 kcal in Tx, Cort, and N respectively. Conclu sions. The present data show that in nondiabetic renal transplant recipient s basal EE is normal. However, basal lipid oxidation is higher and glucose oxidation is lower than in healthy subjects. In addition, the oxidative dis posal of a glucose load and substrate-induced thermogenesis are impaired.