AIM: The acute effects of the oral administration of L-alanine (L-ala), L-glutamine (L-gln), L-ala+L-gln, and L-alanyl-L-glutamine (AGP) on glycemia recovery during short-term insulin-induced hypoglycemia (IIH) were compared. METHODS: For this purpose, the blood glucose levels of 24-h-fasted rats that received intraperitoneal injections of regular insulin (IIH group) or saline [control (COG) group] and, 15 min later, oral administration of L-ala (100 mg/kg), L-gln (100 mg/kg), L-ala (50 mg/kg)+L-gln (50 mg/kg), or AGP (100 mg/kg) were compared. Liver perfusion experiments and blood collection to measure blood glucose levels were performed 30 min after insulin (1.0 U/kg) or saline injection. Livers from the IIH and COG groups were perfused with saturating concentrations of L-ala, L-gln, L-ala+L-gln, or AGP, and the maximal hepatic production of glucose, urea, ammonia, L-lactate, and pyruvate was evaluated. RESULTS: In contrast with L-gln, L-ala+L-gln, or AGP, the oral administration of L-ala promoted glycemia recovery. In agreement with these results, livers from IIH rats showed maximal hepatic production of glucose and urea from L-ala with 50% of the amount used to obtain the maximal hepatic production of glucose and urea in livers from COG rats. In contrast with L-gln, L-ala+L-gln, or AGP, the maximal hepatic production of urea from L-ala occurred in the absence of ammonia accumulation. CONCLUSION: The results indicate that the best glycemia recovery promoted by the oral administration of L-ala was a consequence of the higher efficiency of the livers from IIH rats in producing glucose from L-ala.
AIM: The acute effects of the oral administration of L-alanine (L-ala), L-glutamine (L-gln), L-ala+L-gln, and L-alanyl-L-glutamine (AGP) on glycemia recovery during short-term insulin-induced hypoglycemia (IIH) were compared. METHODS: For this purpose, the blood glucose levels of 24-h-fasted rats that received intraperitoneal injections of regular insulin (IIH group) or saline [control (COG) group] and, 15 min later, oral administration of L-ala (100 mg/kg), L-gln (100 mg/kg), L-ala (50 mg/kg)+L-gln (50 mg/kg), or AGP (100 mg/kg) were compared. Liver perfusion experiments and blood collection to measure blood glucose levels were performed 30 min after insulin (1.0 U/kg) or saline injection. Livers from the IIH and COG groups were perfused with saturating concentrations of L-ala, L-gln, L-ala+L-gln, or AGP, and the maximal hepatic production of glucose, urea, ammonia, L-lactate, and pyruvate was evaluated. RESULTS: In contrast with L-gln, L-ala+L-gln, or AGP, the oral administration of L-ala promoted glycemia recovery. In agreement with these results, livers from IIHrats showed maximal hepatic production of glucose and urea from L-ala with 50% of the amount used to obtain the maximal hepatic production of glucose and urea in livers from COG rats. In contrast with L-gln, L-ala+L-gln, or AGP, the maximal hepatic production of urea from L-ala occurred in the absence of ammonia accumulation. CONCLUSION: The results indicate that the best glycemia recovery promoted by the oral administration of L-ala was a consequence of the higher efficiency of the livers from IIHrats in producing glucose from L-ala.