Effects of metformin on intestinal 5-hydroxytryptamine (5-HT) release and on 5-HT3 receptors

Naunyn Schmiedebergs Arch Pharmacol. 2000 Jan;361(1):85-91. doi: 10.1007/s002109900152.

Abstract

Nearly 30% of patients treated with metformin experience gastrointestinal side effects. Since release of 5-hydroxytryptamine (5-HT) from the intestine is associated with nausea, vomiting, and diarrhea, we examined whether metformin induces 5-HT release from the intestinal mucosa. In 40% of tissue biopsy specimens of human duodenal mucosa, metformin (1, 10, and 30 microM) caused an increase in 5-HT outflow by 35, 70, and 98%, respectively. Peak increases in 5-HT outflow were observed after 10-15 min exposure to metformin, returning to baseline levels after 25 min. Tetrodotoxin (1 microM) reduced by about 50% the metformin-evoked increase in 5-HT outflow (P<0.05). Metformin-evoked release was not affected by scopolamine + hexamethonium, propranolol, the 5-HT3 receptor antagonist dolasetron, naloxone, or the NK1 receptor antagonist L703606. In the presence of tetrodotoxin (1 microM), somatostatin (1 microM) further reduced metformin-induced 5-HT release by 15-20%. In view of the 5-HT releasing effects of selective 5-HT3 receptor agonists to which metformin (N-N-dimethylbiguanide) is structurally related, we investigated whether metformin directly interacts with 5-HT3 receptors. Receptor binding (inhibition of [3H]-GR65630 binding) and agonist effects (stimulation of [14C]-guanidinium influx) at 5-HT3 receptors were studied in murine neuroblastoma N1E-115 cells, which express functional 5-HT3 receptors. Metformin up to 0.3 mM failed to inhibit [3H]-GR65630 binding and to modify displacement of [3H]-GR65630 binding induced by 5-HT. 5-HT (3 microM) stimulated the influx of [14C]-guanidinium in intact N1E-115 cells. Metformin up to 1 mM failed to modify basal influx, 5-HT-induced influx, and 5-HT+ substance P-induced influx of [14C]-guanidinium. Our results indicate that metformin induces 5-HT3 receptor-independent release of 5-HT from human duodenal mucosa via neuronal and non-neuronal mechanisms. Part of the gastrointestinal side effects observed during treatment with metformin could, thus, be produced by the release of 5-HT and other neurotransmitter substances within the duodenal mucosa.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Binding, Competitive / drug effects
  • Cell Membrane / metabolism
  • Chromatography, High Pressure Liquid
  • Duodenum / cytology
  • Duodenum / drug effects
  • Duodenum / metabolism
  • Enterochromaffin Cells / drug effects
  • Enterochromaffin Cells / metabolism
  • Guanidine / metabolism
  • Humans
  • Hypoglycemic Agents / antagonists & inhibitors
  • Hypoglycemic Agents / pharmacology*
  • Imidazoles / metabolism
  • In Vitro Techniques
  • Indoles / metabolism
  • Intestinal Mucosa / cytology
  • Intestinal Mucosa / drug effects
  • Intestinal Mucosa / metabolism*
  • Intestines / cytology
  • Intestines / drug effects
  • Metformin / antagonists & inhibitors
  • Metformin / pharmacology*
  • Mice
  • Neuroblastoma / metabolism
  • Radioligand Assay
  • Receptors, Serotonin / drug effects*
  • Receptors, Serotonin, 5-HT3
  • Serotonin / metabolism*
  • Tumor Cells, Cultured

Substances

  • Hypoglycemic Agents
  • Imidazoles
  • Indoles
  • Receptors, Serotonin
  • Receptors, Serotonin, 5-HT3
  • GR 65630
  • Serotonin
  • Metformin
  • Guanidine