Effects of tryptamine on plasma glucagon levels in mice

Abstract

Our previous study indicated that tryptamine induces a dose-related increase in plasma glucagon levels of mice and that this effect is mediated by the peripheral serotonin2 (5-HT2) receptor. The present paper further investigated the involvement of serotonergic and catecholaminergic systems in hyperglucagonemia elicited by tryptamine. An inhibitor of 5-HT synthesis, p-chlorophenylalanine, did not affect tryptamine-induced increases in plasma glucagon levels. Tryptamine-induced hyperglucagonemia was not inhibited by adrenalectomy or by an inhibition of catecholamine synthesis by alpha-methyl-p-tyrosine. These findings indicate that tryptamine-induced hyperglucagonemia is elicited by its direct activation of 5-HT2 receptors and is not mediated by levels of endogenous 5-HT and catecholamines. The results further suggest that the peripheral 5-HT2 receptor has a possible role in the release of glucagon.

The biogenic amine tryptamine, unlike β-phenylethylamine, shows in vitro cytotoxicity at concentrations that have been found in foods

“…However, very few in vivo studies on acute oral toxicity have been performed. In the reported in vivo experiments performed with laboratory animals, tryptamine was never orally administered (Paley, Denisova, Sokolova, Posternak, Wang, & Brownell, 2007;Yamada, Sugimoto, Kimura, Watanabe, & Horisaka, 1994), and such results cannot be extrapolated to oral ingestion since tryptamine is rapidly metabolized in the gastrointestinal tract by MAO-A and then further in the liver by MAO-B (Wust et al, 2017). In fact, the single reported study on orally administered tryptamine in humans (Honecker, Coper, Fahndrich, & Rommelspacher, 1980) indicates that healthy volunteers who ingested 480 mg of tryptamine per day (160 mg three times per day over three consecutive days) suffered no negative health effects.…”