Hypoglycemia induced by insulin increases hepatic capacity to produce glucose from gluconeogenic amino acids.
AIM
To investigate the hepatic capacity to produce glucose during hypoglycemia induced by insulin (HII).


METHODS
Livers from 24-h fasted rats which received i.p. insulin (HII rats) or saline (control rats) were perfused in situ. 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 gluconeogenic activity was measured as the difference between rates of glucose released during and before the substrate infusion. In part of the experiments the production of urea was measured. Before the liver perfusion blood was collected for determination of glycemia and insulinemia.


RESULTS
HII rats showed: (a) hypoglycemia and hyperinsulinemia; (b) increased hepatic capacity to produce glucose from L-alanine and L-glutamine; (c) increased hepatic ureogenesis from L-alanine and L-glutamine; and (d) increased hepatic glucose production from glycerol. However, hepatic glucose production from L-lactate was not affected by hypoglycemia.


CONCLUSION
In spite of hyperinsulinemia the hepatic capacity to produce glucose from L-glutamine and L-alanine increased during HII. These results can be attributed to the higher hepatic catabolism of both amino acids, since the ability of the liver to produce glucose was not affected by hypoglycemia.