Role of cholinergic muscarinic pathways on the free fatty acid inhibition of GH responses to GHRH in normal men

Clin Endocrinol (Oxf). 1990 Aug;33(2):171-6. doi: 10.1111/j.1365-2265.1990.tb00480.x.

Abstract

In order to explore the mechanisms by which free fatty acids (FFA) inhibit GH secretion, we studied the effect of the acetylcholinesterase inhibitor pyridostigmine (120 mg p.o.) on the FFA blockade of GH responses to the administration of GHRH (100 micrograms i.v.) in seven normal subjects. GHRH-induced GH secretion was significantly reduced following elevation of circulating FFA levels by lipid-heparin infusion and significantly potentiated by previous pyridostigmine treatment. Peak GH levels following combined administration of pyridostigmine plus lipid-heparin plus GHRH were significantly higher (P less than 0.01) than after GHRH alone and significantly lower than after pyridostigmine plus GHRH (P less than 0.01). In conclusion, central cholinergic activation by pyridostigmine, with the presumed reduction in somatostatin discharge, reversed the blocking effect of FFA on GHRH-stimulated GH release. Conversely, FFA were able to reduce even a maximal GH stimulation by pyridostigmine plus GHRH.

Publication types

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

MeSH terms

  • Adult
  • Cholinergic Fibers / physiology*
  • Drug Synergism
  • Fatty Acids, Nonesterified / blood
  • Fatty Acids, Nonesterified / physiology*
  • Feedback / physiology
  • Growth Hormone / blood
  • Growth Hormone / metabolism*
  • Growth Hormone-Releasing Hormone / pharmacology*
  • Humans
  • Male
  • Pyridostigmine Bromide / pharmacology
  • Receptors, Muscarinic / physiology

Substances

  • Fatty Acids, Nonesterified
  • Receptors, Muscarinic
  • Growth Hormone
  • Growth Hormone-Releasing Hormone
  • Pyridostigmine Bromide