THE EFFECT OF SOMATOSTATIN ANALOG ON GLUCOSE-HOMEOSTASIS IN CONSCIOUSDOGS

Our aim was to clarify the effect of a somatostatin analogue (octreoti de) on glucose flux in conscious dogs. We monitored the effects with c atheters in the portal vein, hepatic vein and femoral artery and Doppl er flow probes on the portal vein and hepatic artery before and after oral glucose administration. A significant increase of portal vein pla sma flow after oral glucose was completely suppressed by both 4 and 1 mu g/kg octreotide. All doses of octreotide (4, 1 and 0.1 mu g/kg) sup pressed the glucose-induced increment of arterial glucose by dose resp onse. Only 4 mu g/kg of octreotide slightly but significantly suppress ed hepatic glucose output. Marked suppression and delayed glucose abso rption by the intestine was observed after 4 mu g/kg of octreotide. On e and 0.1 mu g/kg octreotide also suppressed glucose absorption withou t delayed absorption. Total amounts of absorbed glucose during 3 h aft er oral glucose were 24 +/- 11% with 4 mu g/kg of octreotide, 37 +/- 1 6% with 1 mu g/kg of octreotide, and 48 +/- 8% with 0.1 mu g/kg of oct reotide, all of which were significantly less than that of the control (73 +/- 8%). Using 4 mu g/kg of octreotide treatment, the liver took up only 5 +/- 4% of the absorbed glucose, while the liver took up 35 /- 6% and 43 +/- 9% of the absorbed glucose with 1 and 0.1 mu g/kg of octreotide. These latter values were similar to that of the control va lue of 34 +/- 4%. In conclusion, we found that octreotide administered before oral glucose had a remarkable stabilizing effect on postprandi al glycemic surges. Both the direct inhibitory effect of octreotide on portal vein plasma flow and impaired glucose absorption would contrib ute to this decreased postprandial hyperglycemia, while its suppressiv e effect on other hormones, such as insulin and glucagon, did not seem to influence the reduction of hyperglycemia.