Immunoreactive somatostatin (IRS) was measured in extracted plasma obtained from the hepatic portal vein (PV) and inferior vena cava (IVC) of acute, untreated, spontaneously diabetic Wistar rats (BBL), insulin-treated diabetic rats, and nondiabetic controls. Acetic acid extracts of the pancreas and entire gastrointestinal tract were assayed for IRS, and the volume density of pancreatic D-, A-, and B-cells was determined by quantitative morphometry. The concentration of IRS in the PV and IVC of the untreated diabetic rats was significantly elevated compared with controls, with a much greater percent increase in the IVC compared with the PV. Insulin treatment for 4–6 wk restored the elevated PV and IVC levels to control values. The pancreatic content of IRS and the volume density of D-cells was severely reduced in the diabetic groups whereas gut IRS was unchanged. These data suggest that the elevated blood levels are secondary to insulin deficiency and result from altered peripheral metabolism and/or increased secretion of IRS most probably from the gut. The increased peripheral blood concentration of IRS raises the possibility of an endocrine role of circulating somatostatin in diabetes. The reduction in pancreatic IRS found in this model is probably secondary to insulitis and contrasts with the D-cell augmentation reported in streptozotocin-dia-betic rats.

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