1978 Volume 25 Issue 2 Pages 163-169
The intravenous infusion of D-ribose to normal, nonanesthetized and anesthetized dogs at a rate of 3mg/kg·min produced a sustained hypoglycemia. The mean blood glucose concentration decreased to a level about 30mg/dl below the fasting level in 45 min after starting D-ribose infusion and remained at the same level until the infusion was discontinued. After stopping the infusion the blood glucose concentration returned to the preinfusion level in about one hour.
The plasma IRI (immunoreactive insulin) concentration in pancreatic effluent blood in anesthetized dogs increased rapidly, peaked within 5-10 min and then declined gradually, but remained above the basal level during the sustained hypoglycemia.
The plasma IRI concentration in pancreatic effluent blood declined further below the basal level after stopping the infusion. In mixed blood an essentially similar pattern in time course of the plasma IRI concentration was observed in both nonanesthetized and anesthetized dogs.
No change in the plasma IRG (immunoreactive glucagon) concentration in pancreatic effluent blood and the plasma CGH (canine growth hormone) concentration in mixed venous blood was observed during or after the infusion of D-ribose.
The invariable occurrence of hyperinsulinemia during the period of progressive fall of blood glucose and sustained hypoglycemia suggests that insulin release is essential for D-ribose-induced hypoglycemia. Glucagon and growth hormone do not seem to play a role in producing a sustained hypoglycemia to prevent further progress of hypoglycemia by increasing their concentration in the blood. The pattern of insulin release during D-ribose infusion suggests the occurrence of the suppression of D-ribose-stimulated insulin release by the fall of blood glucose below the fasting level, which produces a sustained hypoglycemia at a certain level.
