The diabetogenic effect of prolactin observed in patients with pathological hyperprolactinaemia was verified in healthy subjects. Plasma prolactin elevation was induced by administration of a dopamine antagonist drug domperidone (Motilium 10 mg orally, 9 subjects) and 2 h later the oral glucose tolerance test was performed. The influence of dopamine receptor stimulation on glucose homeostasis was tested by dopamine infusion (0.3 mg in saline or 20 % glucose, 1 g/min for 60 min, 11 subjects). After the blockade of dopamine receptors, a significant and prolonged increase of prolactin concentration was found. However, the levels of glucose, insulin, and C- peptide either before or after the glucose load were not different from control ones. The decreased number of insulin receptors (1.97±0.41 vs 0.51 ±0.14 pmol per 2.109 red blood cells) was compensated by increased affinity (0.51 ±0.17 vs 1.00±0.22 K* 108 mol.-1 per 1]) of insulin receptors. The stimulation of dopamine receptors showed a negligible effect on glucose regulation. It may be suggested that an endogenous increase of prolactin concentration in the physiological range does not participate in the regulation of glucose homeostasis in healthy subjects.
We evaluated the effects of 2.5xlO-10 M or 5xlO-10 M concentrations of human pituitary prolactin (pPRL), human recombinant non-glycosylated (NG-PRL) and glycosylated (GL-PRL) prolactin on the proliferation of normal human lymphocytes with or without coactivation by interleukin-2 (IL-2). None of the PRL forms alone affected the lymphocyte proliferation in a serum-free medium, however, the stimulatory activity of IL-2 was significantly potentiated with all 3 PRL variants. Since the 5xlO~10 M concentrations of individual PRLs exerted the same effects, this result suggests that GL-PRL in primary lymphocyte culture is not a less mitogenic form, if sufficient amounts of IL-2 are available.
Activation of the hypothalamic-pituitary-adrenal (HPA) axis is important for maintenance of homeostasis during stress. Recent studies have shown a connection between the HPA axis and adipose tissue. The present study investigated the effect of acute heterotypic stress on plasma levels of adrenocorticotropic hormone (ACTH), corticosterone (CORT), leptin, and ghrelin in adult male rats with respect to neonatal maternal social and physical stressors. Thirty rat mothers and sixty of their male progeny were used. Pups were divided into three groups:
unstressed control (C), stressed by maternal social stressor (S),
stressed by maternal social and physical stressors (SW). Levels of
hormones were measured in adult male progeny following an
acute swimming stress (10min) or no stress. ELISA immunoassay was used to measured hormones. The ACTH and CORT levels were significantly increased in all groups of adult progeny after acute stress; however, CORT levels were significantly lower in both neonatally stressed groups compared to controls. After acute stress, plasma leptin levels were decreased in the C and SW groups but increased in the S group. The data suggest that long-term neonatal stressors lead to lower sensitivity of ACTH receptors in the adrenal cortex, which could be a sign of stress adaptation in adulthood. Acute stress in adult
male rats changes plasma levels of leptin differently relative to social or physical neonatal stressors.