Glucose generates coincident insulin and somatostatin pulses and antisynchronous glucagon pulses from human pancreatic islets

Endocrinology. 2009 Dec;150(12):5334-40. doi: 10.1210/en.2009-0600. Epub 2009 Oct 9.


The kinetics of insulin, glucagon and somatostatin release was studied in human pancreatic islets. Batches of 10-15 islets were perifused and the hormones measured with RIA in 30-sec fractions. Increase of glucose from 3 to 20 mm resulted in a brief pulse of glucagon coinciding with suppression of basal insulin and somatostatin release. There was a subsequent drop of glucagon release concomitant with the appearance of a pronounced pulse of insulin and a slightly delayed pulse of somatostatin. Continued exposure to 20 mm glucose generated pulsatile release of the three hormones with 7- to 8-min periods accounting for 60-70% of the secreted amounts. Glucose caused pronounced stimulation of average insulin and somatostatin release. However, the nadirs between the glucagon pulses were lower than the secretion at 3 mm glucose, resulting in 18% suppression of average release. The repetitive glucagon pulses were antisynchronous to coincident pulses of insulin and somatostatin. The resulting greater than 20-fold variations of the insulin to glucagon ratio might be essential for minute-to-minute regulation of the hepatic glucose production.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Animals
  • Cadaver
  • Dose-Response Relationship, Drug
  • Female
  • Glucagon / metabolism*
  • Glucose / pharmacology*
  • Humans
  • Insulin / metabolism*
  • Insulin Secretion
  • Islets of Langerhans / drug effects*
  • Islets of Langerhans / metabolism
  • Male
  • Middle Aged
  • Radioimmunoassay
  • Somatostatin / metabolism*
  • Time Factors


  • Insulin
  • Somatostatin
  • Glucagon
  • Glucose