Sensitivity to beta-endorphin as a cause of human obesity

Metabolism. 1987 Oct;36(10):974-8. doi: 10.1016/0026-0495(87)90135-1.

Abstract

Naloxone, an opiate antagonist, was given as an intravenous bolus (5 mg) in both lean and obese healthy subjects. In lean people, there was a slight trend for insulin and C-peptide concentrations to decrease below baseline values with no glucose change. Obese subjects showed an exaggerated suppression of insulin and C-peptide and a slight decrease of glucose. Glucagon was suppressed in both groups. An infusion of human beta-endorphin (0.05 mg/h) produced only minor changes in plasma glucose, insulin, glucagon, and C-peptide concentrations in lean subjects, but caused marked increments in obese. Glucagon rose in both groups, but its response was greater in obese subjects. A ten-day treatment with naloxone (1.2 mg twice a day) did not change the metabolic and hormonal responses to an oral glucose load (75 g) in lean but significantly inhibited the insulin and C-peptide responses to glucose in obese people. These results suggest that an increased opiate drive to the pancreatic beta-cell and an increased responsiveness of insulin to beta-endorphin are present in human obesity.

MeSH terms

  • Adult
  • Blood Glucose / metabolism
  • C-Peptide / blood
  • Female
  • Glucagon / blood
  • Glucose Tolerance Test
  • Humans
  • Insulin / blood
  • Islets of Langerhans / drug effects
  • Islets of Langerhans / physiopathology*
  • Male
  • Naloxone / pharmacology
  • Obesity / blood
  • Obesity / physiopathology*
  • beta-Endorphin / pharmacology
  • beta-Endorphin / physiology*

Substances

  • Blood Glucose
  • C-Peptide
  • Insulin
  • Naloxone
  • beta-Endorphin
  • Glucagon