Impaired glucose oxidation and glucose-induced thermogenesis in renal transplant recipients.
BACKGROUND
Renal transplant recipients often show various metabolic abnormalities including reduced glucose tolerance, impaired insulin sensitivity and altered lipid metabolism. However, the acute effects of carbohydrate ingestion on substrate utilization and energy expenditure have not been fully elucidated.


METHODS
We evaluated: (i) basal energy expenditure (EE) and substrate utilization, (ii) metabolic fate of an oral glucose load, and (iii) substrate-induced thermogenesis in: (a) 15 non-diabetic renal transplant recipients (Tx) (BMI 25+/-1) on triple immunosuppressive therapy, (b) 11 patients with primary glomerulonephritis (BMI 25+/-1) (Cort) receiving prednisone treatment, and (c) 12 healthy subjects (BMI 26+/-1) (N). Continuous indirect calorimetry was performed in the basal post-absorptive state for 60 min and continued 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 averaged 14.6+/-0.7, 15.7+/-1.3, and 14.1+/-0.8 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 and vs. Cort), whereas lipid oxidation was lower in N (0.6+/-0.1 mg/kg/min) than in Tx (0.9+/-0.1) and Cort (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.


CONCLUSIONS
The present data show that in non-diabetic renal transplant recipients basal EE is normal. However, basal lipid oxidation is higher and glucose oxidation is lower than in healthy subjects. In addition, the oxidative disposal of a glucose load and substrate-induced thermogenesis are impaired.
de Pascale
E
E
Istituto di Clinica Medica Generale e Terapia Medica 'L. Condorelli' Universita' di Catania, Istituto di Medicina Interna e Nefrologia e. Istituto di Endocrinologia, Seconda Universita' di Napoli, Italy.
Giordano
M
M
Carone
M
M
Pluvio
C
C
Pluvio
M
M
Criscuolo
T
T
Infantone
L
L
Castellino
P
P
D000284:Administration, Oral; D000328:Adult; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D001786:Blood Glucose / Q000032:analysis; D002153:Calorimetry, Indirect; D050260:Carbohydrate Metabolism; D004359:Drug Therapy, Combination; D004734:Energy Metabolism; D005260:Female; D005921:Glomerulonephritis / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology; D005947:Glucose / Q000378:metabolism / Q000494:pharmacology / Q000502:physiology*; D006801:Humans; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D007328:Insulin / Q000097:blood; D016030:Kidney Transplantation; D050356:Lipid Metabolism; D008297:Male; D010084:Oxidation-Reduction; D011241:Prednisone / Q000627:therapeutic use; D012016:Reference Values; D022722:Thermogenesis
D000893:Anti-Inflammatory Agents; D001786:Blood Glucose; D007166:Immunosuppressive Agents; D007328:Insulin; D005947:Glucose; D011241:Prednisone