Evidence that the accumulation of 5-hydroxytryptamine in the liver but not in the brain may cause the hypoglycaemia induced by 5-hydroxytryptophan.
Experiments were undertaken to determine whether the site of the hypoglycaemic action of 5-hydroxytryptophan (5-HTP), a direct precursor of 5-hydroxytryptamine (5-HT), was in the central nervous system or in the liver. The fall in blood glucose followed the rapid increase in the amount of 5-HT both in the brain and liver after 5-HTP injection into pargyline-treated and non-treated mice. Carbidopa, an inhibitor of peripheral aromatic amino acid decarboxylase, prevented the elevation of 5-HT levels in the liver of both pargyline-treated and non-treated mice. In contrast, carbidopa did not prevent but rather enhanced the elevation of 5-HT levels in the brain of both groups of mice. Corresponding to the prevention of 5-HT elevation in the liver, the fall in blood glucose was prevented by carbidopa. These results support the idea that the accumulation of 5-HT in the liver but not in the brain causes the hypoglycaemia induced by 5-HTP.
D006916:5-Hydroxytryptophan / Q000494:pharmacology*; D000818:Animals; D001921:Brain / Q000187:drug effects / Q000378:metabolism*; D002230:Carbidopa / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D007003:Hypoglycemia / Q000139:chemically induced* / Q000378:metabolism; D008099:Liver / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D051379:Mice; D010293:Pargyline / Q000494:pharmacology; D012701:Serotonin / Q000378:metabolism*; D013997:Time Factors
D012701:Serotonin; D010293:Pargyline; D006916:5-Hydroxytryptophan; D002230:Carbidopa