ACUTE ELEVATION OF ENDOGENOUS PROLACTIN DOES NOT INFLUENCE GLUCOSE-HOMEOSTASIS IN HEALTHY-MEN

The diabetogenic effect of prolactin observed in patients with patholo gical hyperprolactinaemia was verified in healthy subjects. Plasma pro lactin elevation was induced by administration of a dopamine antagonis t drug domperidone (Motilium 10 mg orally, 9 subjects) and 2 h later t he oral glucose tolerance test was performed. The influence of dopamin e receptor stimulation on glucose homeostasis was tested by dopamine i nfusion (0.3 mg in saline or 20 % glucose, 1 g/min for 60 min, 11 subj ects). After the blockade of dopamine receptors, a significant and pro longed increase of prolactin concentration was found. However, the lev els of glucose, insulin, and C-peptide either before or after the gluc ose load were not different from control ones. The decreased number of insulin receptors (1.97+/-0.41 vs 0.51+/-0.14 pmol per 2.10(9) red bl ood cells) was compensated by increased affinity (0.51+/-0.17 vs 1.00/-0.22 K-e 10(8) mol.(-1), per l]) of insulin receptors. The stimulati on of dopamine receptors showed a negligible effect on glucose regulat ion. It may be suggested that an endogenous increase of prolactin conc entration in the physiological range does not participate in the regul ation of glucose homeostasis in healthy subjects.