Antidiabetic Action of Somatostatin after Oral Glucose Loading: Due to Suppression of Glucagon and Growth Hormone or of Intestinal Carbohydrate Absorption?

Summary

To elucidate the mechanism by which somatostatin lowers blood glucose concentration and insulin requirement following carbohydrate ingestion in insulin dependent diabetic patients (IDDM; n = 6), the amount of insulin required for the assimilation of a 50 g glucose load was determined by means of an automated glucose-controlled insulin infusion system with and without concomitant somatostatin infusion. During the 3 hour period following glucose loading plasma concentrations of glucagon and growth hormone were diminished by somatostatin, as were the rise in blood glucose and insulin requirement (4.0 ± 1.2 U) when compared with the control study (11.3 ± 1.5 U; p < 0.01). With cessation of somatostatin blood glucose levels and insulin requirement rose during the following 2 hour observation period (7.5 ± 1.2 U) but remained basal during the control study (0.7 ± 0.6 U; p < 0.0005). Thus the integrated amounts of insulin required for glucose assimilation were nearly identical whether or not glucagon and growth hormone were temporarily suppressed by somatostatin. It is concluded that the diminished insulin requirement and delayed rise in blood glucose during somatostatin administration after an oral glucose load is not due toits “antidiabetic” action by suppressing glucagon and growthhormone release. Our findings favour inhibition of intestinal carbohydrate absorption as the determining cause for the “antidiabetic” action of somatostatin.

Key-Words:

Somatostatin - Glucagon - Growth Hormone - Diabetes Mellitus - Glucose - Artificial Endocrine Pancreas - Insulin Requirement