E. Virasoro

SIMULTANEOUS STUDY OF CORTISOL, GROWTH HORMONE AND PROLACTIN NYCTOHEMERAL VARIATIONS IN NORMAL AND OBESE SUBJECTS. INFLUENCE OF PROLONGED FASTING IN OBESITY

Hourly integrated concentrations (IC) of growth hormone (GH), prolactin (PRL) and cortisol were determined by a continuous sampling procedure in six obese women, before and at the end of a 12 day fast, and in eight normal controls under basal conditions. Hormonal 24 h IC and nyctohemeral variations were calculated from these data. Nyctohemeral rhythms were investigated by the periodogram method.

ACUTE ENDOCRINE PROFILE OF SULPIRIDE IN THE HUMAN

Normal men and normally menstruating women received i.m. injections of 0.1 to 4.0 mg/kg sulphide. This psychotropic drug induced a very rapid (already significant after 5 minutes) and sustained (still significant after 7 hours) elevation of prolactin (PRL) concentrations in all subjects with no consistent modification of LH and FSH. After injection of 4.0 mg/kg, there was similarly no modification of mean TSH concentrations in the women tested in the luteal phase, as well as of mean GH levels in men. Sulpiride prevented the inhibitory effect on PRL levels of 500 mg levodopa, administered orally simultaneously; levodopa administered 2 hours prior to sulpiride failed to counteract the PRL‐stimulatory effect of sulpiride. Under chronic sulpiride‐induced hyperprolactinaemia, levodopa exhibited however a very slight inhibitory effect on PRL concentrations. These data are in agreement with the hypothesis that sulpiride acts mainly at the pituitary level by blocking dopamine receptors of the lactotropes and support the concept that the menstrual cycle perturbations observed under chronic sulpiride administration result from hyperprolactinaemia itself or from a mechanism quite similar to that by which sulpiride induces hyperprolactinaemia.

Specific inhibition by somatostatin of growth hormone release after hypoglycaemia in normal man

In normal man, synthetic linear somatostatin (growth hormone‐release inhibiting hormone) inhibits the growth hormone response to insulin induced hypoglycaemia, but has no influence on plasma levels of cortisol, prolactin, TSH and FSH.