Somatostatin and oxytocin infusion inhibits the rise of plasma beta-endorphin, beta-lipotrophin and cortisol induced by insulin hypoglycaemia

Clin Endocrinol (Oxf). 1986 Jun;24(6):609-16. doi: 10.1111/j.1365-2265.1986.tb01656.x.

Abstract

The present study investigated the possible effect of somatostatin and oxytocin on the basal and stress-induced rise of beta-endorphin (beta-END), beta-lipotrophin (beta-LPH) and cortisol in the human. For this purpose somatostatin (4.1 micrograms/min for 120 min or oxytocin (0.4 micrograms/min for 120 min) was infused into two different groups of seven healthy subjects; 30 min after the start of the infusion, placebo or insulin (0.1 IU/kg body weight, B.W.) was injected on two different days. In a third experimental step, an insulin tolerance test was performed during saline infusion to evaluate stress-related effects on the different hormonal secretions under basal conditions. Plasma levels of beta-END, beta-LPH and cortisol were measured by radioimmunoassay. Extraction and chromatographic procedures preceded the assay for beta-END and beta-LPH. Neither somatostatin nor oxytocin significantly modified basal plasma levels of beta-END, beta-LPH and cortisol. However these treatments blunted the rise of the three hormones seen at 45 and 60 min during insulin-induced hypoglycaemia (P less than 0.01). These results indicate that somatostatin and oxytocin may influence the beta-END, beta-LPH and cortisol increase induced by stress in humans, without affecting their basal secretion.

Publication types

  • Clinical Trial
  • Randomized Controlled Trial
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Depression, Chemical
  • Endorphins / blood*
  • Female
  • Humans
  • Hydrocortisone / blood*
  • Hypoglycemia / blood*
  • Male
  • Oxytocin / pharmacology*
  • Somatostatin / pharmacology*
  • beta-Endorphin
  • beta-Lipotropin / blood*

Substances

  • Endorphins
  • Oxytocin
  • Somatostatin
  • beta-Endorphin
  • beta-Lipotropin
  • Hydrocortisone