Truncal vagotomy abolishes the somatostatin response to insulin-induced hypoglycemia in man

The mechanism whereby insulin-induced hypoglycemia stimulates release of immunoreactive somatostatin (SRIF-LI) into the peripheral circulation in man is unknown. We have measured the plasma SRIF-LI response to insulin-induced hypoglycemia in 16 healthy subjects and five subjects with prior truncal vagotomy. Mean nadir of plasma glucose was similar in the two groups (37 +/- 5 and 34 +/- 2 mg/dl in the control group). Hypoglycemia induced a brisk rise in plasma pancreatic polypeptide (hPP) concentrations in healthy subjects (maximum concentration 1563 +/- 245 pg/ml) whereas in none of the postvagotomy subjects was there a significant change in hPP concentrations, indicative of completeness of the truncal vagotomy. In healthy subjects SRIF-LI concentrations rose for a basal of 168 +/- 19 pg/ml to a maximum of 254 +/- 30 at 39 +/- 4 minutes (p less than 0.005) with an incremental area of 2.8 +/- 1 ng . min/ml above basel. In vagotomized subjects, the mean basal SRIF-LI concentration of 166 +/- 22 pg/ml was not significantly different from that in healthy subjects. After insulin injection, SRIF-LI concentration fell with a net decrement of -3.2 +/- 1 ng . min /ml below the basal. It is concluded that the SRIF-LI response to insulin-induced hypoglycemia is dependent upon vagal integrity. Section of the vagus unmasks a suppressive effect of insulin action or its metabolic or hormonal consequences on the concentration of SRIF-LI in plasma.