Acute hypoglycemia in man: neural control of pancreatic islet cell function

Acute hypoglycemia is associated with stimulation of the pancreatic alpha cells and a concurrent, prolonged suppression of insulin secretion by the beta cells. The islets receive a rich autonomic innervation and may therefore be subject to control by adrenergic and cholinergic mechanisms. The role of such neuroregulation of pancreatic islets in response to hypoglycemia has been examined in normal subjects, in subjects with a preganglionic sympathectomy due to traumatic tetraplegia, and in tetraplegic subjects given atropine to induce effective dual autonomic denervation. The normal rise of plasma norepinephrine following hypoglycemia was absent in both groups of tetraplegic subjects, providing evidence of a complete sympathectomy. Blood glucose recovery was significantly impaired only in the group of tetraplegic patients given atropine. Changes in plasma C-terminal glucagon-like immunoreactivity (C-GLI) and C-peptide immunoreactivity (CPR) following hypoglycemia were commensurate with blood glucose levels and were not significantly influenced by islet denervation. These observations suggest that neuroregulation of human islet cell function in response to hypoglycemia may be of limited importance and that stimulation of glucagon secretion may occur independent of cholinergic vagal control.