Hypoglycemia induced by insulin increases hepatic capacity to produce glucose from gluconeogenic amino acids

AIM: To investigate the hepatic capacity to produce glucose during hypoglyc emia induced by insulin (HII). METHODS: Livers from 24-h fasted rats which received ip insulin (HII rats) or saline (control mts) were perfused in sit u. The gluconeogenic substrates L-alanine (5 mmol/L), L-glutamine (5 mmol/L ), L-lactate (2 mmol/L), and glycerol (2 mmol/L) were employed. The glucone ogenic activity was measured as the difference between rates of glucose rel eased during and before the substrate infusion. In part of the experiments the production of urea was measured. Before the liver perfusion blood was c ollected fbr determination of glycemia and insulinemia. RESULTS: HII rats s howed: (a) hypoglycemia and hyperinsulinemia; (b) increased hepatic capacit y to produce glucose from L-alanine and L-glutamine; (c) increased hepatic ureogenesis from L-alanine and L-glutamine; and (d) increased hepatic gluco se production from glycerol. However, hepatic glucose production from L-lac tate was not affected by hypoglycemia. CONCLUSION: In;spite of hyperinsulin emia the hepatic capacity to produce glucose from L-glutamine and L-alanine increased during HII. These results can be attributed to the higher hepati c catabolism of both amino acids, since the ability of the liver to produce glucose was not affected by hypoglycemia.