Prolactin

About: Prolactin is a research topic. Over the lifetime, 22356 publications have been published within this topic receiving 609537 citations. The topic is also known as: lactotropin, & PRL,.

Divergent effects of estradiol on gonadotropin gene transcription in pituitary fragments.

Abstract: Our previous work demonstrated that in vivo estradiol (E2) administration to ovariectomized rats suppressed the transcription of the LH subunit genes within 4 h. To determine whether these effects were mediated directly at the level of the gonadotrope, the transcription rates of the LHβ, FSHβ, and α-subunits were measured in short term cultures of pituitary fragments from female rats in various physiological states. In each in vitro experiment, fragments from matched sets of hemipituitaries were used for control and treatment (10−8mE2) groups. In pituitaries from ovariectomized animals, treated in vitro with or without E2, there was no significant effect of 2 h or 6 h of E2 on FSHβ or α-subunit gene transcription, but a consistent 2- to 3-fold stimulation of LHβ mRNA synthesis. In pituitaries from intact randomly cycling rats, E2 in culture had no effect on the transcription rate of α-subunit, FSHβ, or TSHβ genes, but stimulated LHβ and PRL transcription 2- fold. Thyroid hormone treatment specifically sup...

d-fenfluramine/prolactin response throughout the menstrual cycle: evidence for an oestrogen-induced alteration.

Abstract: The prolactin (PRL) response to fenfluramine (FEN), a serotonin (5-HT) releasing agent, is used as an index of 5-HT sensitivity in studying disorders associated with central 5-HT abnormality. Plasma oestrogen levels are known to augment PRL responses to a variety of stimuli. In order to examine the effect that ovarian steroids have on this response nine, healthy women were tested twice at three time points in the menstrual cycle: early follicular, mid-cycle and late luteal phase with either d-FEN, a more specific 5-HT agent than the racemic mixture, or placebo. Responses to d-FEN were maximal at mid-cycle, lowest during the early follicular phase, with responses premenstrually being intermediate between the two. Responses to placebo did not vary. Plasma oestradiol levels fluctuated in parallel with neuroendocrine responses to d-FEN. The possible mechanisms are discussed, including an effect that oestradiol may exert at central serotonin sites.

Effects of steroid and lactogenic hormones on islets of Langerhans: a new hypothesis for the role of pregnancy steroids in the adaptation of islets to pregnancy

Abstract: Adaptive changes that occur in islets of Langerhans during pregnancy include enhanced insulin secretion, insulin synthesis, beta-cell proliferation, gap-junctional coupling among beta-cells, and glucose oxidation We have determined that elevated lactogenic activity is directly responsible for these changes in beta-cell function Recently, we showed that two of the principal adaptive characteristics (insulin secretion and beta-cell proliferation) of rat pregnancy peaked on day 15 and returned to control levels by day 20 As placental lactogen remains elevated during late gestation, it was of interest to determine whether pregnancy steroids could reverse the effects of lactogen on islets In this study, rat islets were cultured with progesterone, estradiol, rat PRL (rPRL), or combinations of these hormones (progesterone and rPRL, estradiol and rPRL, or progesterone and estradiol and rPRL) Insulin secretion was examined for 8 days, and beta-cell proliferation by 2-bromo-5'-deoxyuridine (BrdU) incorporation

Insulin suppresses growth hormone secretion by rat pituitary cells.

Abstract: The effects of insulin on basal and hydrocortisone-induced growth hormone (GH) secretion were studied in rat pituitary tumor cells (GH3). Cells were grown in monolayer culture and exposed to exogenously added insulin for up to 8 d. Basal GH secretion was inhibited by insulin (0.7 nM) after a 48-h lag period by approximately 50% (P less than 0.01, vs. untreated control cells). The suppression of GH secretion was reversible, as removal of added insulin resulted in return of GH secretion to normal levels after 24 h. Maximal suppression of basal GH secretion was achieved by 0.7 nM insulin, and these effects were prevented by simultaneous exposure of the cells to guinea pig anti-insulin serum (1:2,000). No effects of insulin on cell replication were evident, and glucose concentration in the medium did not differ in control or insulin-treated wells. Insulin (7 nM) significantly suppressed the fivefold hydrocortisone-induced GH stimulation during 5 d of incubation with up to 1,000 nM of the steroid (P less than 0.001). These inhibitory effects were similarly observed in glucose- and pyruvate-free medium, and in the presence of 2-deoxyglucose. Insulin also reversed the suppression of prolactin (PRL) secretion induced by hydrocortisone (1 uM), and actually stimulated basal PRL secretion by over 50%. Insulin did not alter the inhibitory effect of hydrocortisone on GH3 cell proliferation. Although higher doses (13 nM) of insulin-like growth factor (IGF-I) also suppressed basal GH secretion, IGF-I did not alter the GH and PRL secretory changes induced by hydrocortisone. The results show that insulin exerts a direct, specific inhibitory effect on basal and hydrocortisone-induced GH secretion by GH3 cells unrelated to glucose utilization by the cells.