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SUMMARY The relation between hepatic glucose production rate (HGPR) and plasma concentrations of insulin and glucagon was investigated in four term neonates who had severe hypoglycaemia. The hepatic glucose production rate was less than 20% of normal for fasting term neonates in all four babies and yet insulin concentrations were never >12 tU/ml; two babies had very low glucagon concentrations (<60 ng/l). Two further neonates with similar histories also had plasma glucagon concentrations that were also extremely low (<20 ng/l). A single intravenous bolus of glucagon caused a rapid rise in hepatic glucose production rate towards the normal range, which was sustained for many hours after the bolus had been given. Diazoxide given to one baby suppressed previously 'normal' insulin concentrations still further (4.2 to <1-6 [tU/ml) and thereby restored the hepatic glucose production rate to normal. In view of the normal plasma insulin concentrations at a time when the hepatic glucose production rate was reduced, we feel that the absolute concentration of insulin may be less important than the insulin/glucagon molar ratio in the control of glucose homeostasis in this group of infants. The changing of this ratio by means of boluses of glucagon may be useful in preventing rebound hypoglycaemia, which so often occurs when dextrose infusions are reduced either accidentally or in an attempt to restart oral feeds.Although hypoglycaemia is a well recognised complication in babies who are preterm or small for gestational age, it can also occur in term neonates who are otherwise well. In these babies it is often a severe problem in terms of clinical management. Many of them have no obvious disorder such as an inherited metabolic disease or maternal diabetes mellitus to explain their low plasma glucose concentration and yet they often require more than 55 ,mol/kg/min of intravenous dextrose to prevent hypoglycaemia (normal range 27-44 [tmol/kg/min).This extremely high rate of dextrose infusion sets this group of infants apart from others with hypoglycaemia because of their inability to maintain euglycaemia during even the shortest of fasts or during 'normal' rates of glucose infusion.They may still have an extremely labile plasma glucose concentration, despite being given dextrose intravenously, and often have convulsions if the rate of infusion falls suddenly, which may occur when the drip tissues. It is often assumed that the hypoglycaemia is due to 'hyperinsulinism',1 but the exact relation between plasma insulin concentration and rate of glucose production and release from the liver remains unclear.This relation has been studied in six infants (

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