L-tryptophan and neuroendocrine regulation in neurologic patients: hormone responses to L-tryptophan loading in patients with hypothalamic lesions

1. Oral administration of 2 g of l-tryptophan induced a marked plasma elevation of total and free tryptophan during the 2 hr of sampling in both normal subjects and in neurologic patients. Plasma free trytophan concentration showed a peak about 60 min after loading with l-tryptophan. 2. Plasma immunoreactive follitrophin (FSH) and lutrophin (LH) levels were not altered after l-tryptophan treatment. 3. Plasma immunoreactive somatotrophin (growth hormone, GH) levels showed a statistically significant elevation after l-tryptophan loading in both normal subjects and in neurologic control patients. In two acromegalic patients there was a very marked elevation of plasma somatotrophin levels 90 min after loading. No responses of plasma somatotrophin to l-tryptophan were observed in patients with hypothalamic lesion or with hypopituitarism. 4. Plasma cortisol levels showed significant morning decline during loading either with l-tryptophan or with l-leucine as placebo in normal subjects and in neurologic control patients. In patients with hypothalamic lesion the monitoring of plasma cortisol concentrations during l-tryptophan loading revealed a primary elevation with a subsequent slight decline. No variation of plasma cortisol was found in patients with hypopituitarism. 5. It was concluded that the brain serotoninergic system can be activated by l-tryptophan treatment which results in alterations of the hypothalamic regulation of somatotrophin secretion. When neuroendocrine dysfunction is due to structural lesions in the hypothalamus or in related regions, l-tryptophan loading is unable to modify somatotrophin secretion. The normal morning decline of plasma cortisol levels is lacking in such patients.