A fall in portal vein insulin does not cause the alpha-cell response to mild, non-insulin-induced hypoglycemia in conscious dogs

Metabolism. 2003 Nov;52(11):1418-25. doi: 10.1016/s0026-0495(03)00321-4.

Abstract

The aim of the present study was to determine whether a decrease in the portal vein insulin level during non-insulin-induced hypoglycemia is sensed and is responsible for the normal increase in glucagon release from the alpha cell. To address this aim, a glycogen phosphorylase inhibitor was used to create mild, non-insulin-induced hypoglycemia in 2 groups of 18-hour fasted conscious dogs. Arterial insulin was clamped at a basal level in both groups, but in one group (PE) the portal vein insulin level was permitted to fall by approximately 65% while in the other group (POR) it was clamped at a basal level. In both groups glucose was infused at a variable rate to clamp the plasma glucose level at approximately 70 mg/dL. Plasma glucagon (pg/mL) rose to indistinguishable maxima in both groups (56 +/- 3 in PE and 67 +/- 9 in POR). Likewise, glucagon secretion (pg/kg/min) increased similarly (189 +/- 32 to 455 +/- 203 in PE and 192 +/- 50 to 686 +/- 237 in POR). Thus, the increase in glucagon release was not inhibited when the portal vein insulin level was prevented from decreasing (POR group). Clearly, a fall in the portal vein insulin level is not required for a normal alpha-cell response to mild, non-insulin-induced hypoglycemia.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Biosensing Techniques
  • Blood Glucose / metabolism
  • C-Peptide / blood
  • Dogs
  • Female
  • Glucagon / blood
  • Glucagon / metabolism
  • Glycogen Phosphorylase / metabolism
  • Hypoglycemia / metabolism*
  • Insulin / blood*
  • Islets of Langerhans / physiology*
  • Male
  • Norepinephrine / blood
  • Portal Vein / metabolism*

Substances

  • Blood Glucose
  • C-Peptide
  • Insulin
  • Glucagon
  • Glycogen Phosphorylase
  • Norepinephrine