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.