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,.

Elevated luteinizing hormone induces expression of its receptor and promotes steroidogenesis in the adrenal cortex

Abstract: Transgenic (TG) female mice expressing bLHβ-CTP (a chimeric protein derived from the β-subunit of bovine luteinizing hormone [LH] and a fragment of the β-subunit of human chorionic gonadotropin [hCG]) exhibit elevated serum LH, infertility, polycystic ovaries, and ovarian tumors. In humans, increased LH secretion also occurs in infertility and polycystic ovarian syndrome, often concomitant with adrenocortical dysfunction. We therefore investigated adrenal function in LH overexpressing bLHβ-CTP female mice. The size of their adrenals was increased by 80% with histological signs of cortical stimulation. Furthermore, adrenal steroid production was increased, with up to 14-fold elevated serum corticosterone. Primary adrenal cells from TG and control females responded similarly to ACTH stimulation, but, surprisingly, the TG adrenals responded to hCG with significantly increased cAMP, progesterone, and corticosterone production. LH receptor (LHR) expression and activity were also elevated in adrenals from female TG mice, but gonadectomized TG females showed no increase in corticosterone, suggesting that the dysfunctional ovaries of the intact TG females promote adrenocortical hyperfunction. We suggest that, in intact TG females, enhanced ovarian estrogen synthesis causes increased secretion of prolactin (PRL), which elevates LHR expression. Chronically elevated serum LH, augmented by enhanced PRL production, induces functional LHR expression in mouse adrenal cortex, leading to elevated, LH-dependent, corticosterone production. Thus, besides polycystic ovaries, the bLHβ-CTP mice provide a useful model for studying human disorders related to elevated LH secretion and adrenocortical hyperfunction.

Relationship Between LH, FSH, and Prolactin Concentration and the Secretion of Androgens and Estrogens by the Preovulatory Follicle in the Ewe

Abstract: The ovarian secretion of estradiol, androstenedione, testosterone, and progesterone and the concentration of LH, FSH, and prolactin were measured in the periovulatoiy period of five ewes with ovarian or utero-ovarian autotransplants Samples of jugular and ovarian venous blood were collected every 1 or 2 h before and for 96 h after induction of luteal regression on Day 10 of the cycle by injection of 100 �zg cloprostenol Progesterone concentration in jugular vein plasma fell to less than 1 ng/ml in all ewes by 24 h, and coincidental to this decline there was a significant increase in the secretion of LH and prolactin and an associated rise in the ovarian venous concentration of estradiol, testosterone, and androstenedione The rise in LH secretion was associated with a twofold increase in the frequency of episodic pulses each of which stimulated an increase in the secretion of estradiol In contrast the concentration of FSH declined significantly in the 48 h after luteal regression Shortly after the onset of estrus (48 ± 25 h), there was a marked rise in the concentration of prolactin, FSH, and LH which reached a peak at 61 ± 4 h At the start of this preovulating LH surge, there was a further substantial stimulation in the secretion of estradiol, testosterone, and androstenedione, followed by a sharp fall within 3, 5, and 7 h, respectively In the 24 h after the preovulatory surge, there was a marked decline in the concentration of LH and prolactin as well as all ovarian steroids However, within 12 h there was a further rise in the concentration of FSH which reached a second peak at 23 h after the LH peak These results suggest that the increased secretion of estradiol from the preovulatory follicle is due to stimulation by episodic pulses of LH which occur with increased frequency as the concentration of progesterone falls during luteal regression The sustained rise in LH which occurs during the preovulatory surge stimulates and then markedly inhibits aromatase activity and eventually all steroid secretion from the follicle Thus the final stages of development of the preovulatory follicle are determined not by FSH but by the pattern of secretion of LH

New concepts in prolactin biology

Abstract: Human prolactin (PRL) is currently viewed as a hormone of pituitary origin, whose production (i.e. serum levels) is controlled by dopamine, whose biological actions relate exclusively to lactation and reproductive functions, for which any genetic disorder is yet to be identified, and whose unique associated pathology is hyperprolactinemia. Both experimental studies and human sample/cohort-based investigations performed during the past decade have considerably widened our perception of PRL biology: i) there are now strong epidemiological arguments supporting the fact that circulating PRL is a risk factor for breast cancer, ii) in addition to the endocrine hormone, locally produced PRL has been documented in several human tissues; there is increasing evidence supporting the tumor growth potency of local PRL, acting via autocrine/paracrine mechanisms, in both rodent models, and human breast and prostate tumors, iii) the first functional germinal polymorphisms of the PRL receptor were recently identified in patients presenting with breast tumors, which involve single amino acid substitution variants exhibiting constitutive activity, iv) human PRL analogs have been engineered, which were shown in experimental models to down-regulate the effects triggered by local PRL (competitive antagonism) or by the constitutively active receptor variants (inverse agonism). The aim of this review is to discuss these novel concepts in PRL biology, including their potential pathophysiological outcomes.