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,.

Epidermal growth factor and thyrotropin-releasing hormone act similarly on a clonal pituitary cell strain. Modulation of hormone production and inhibition of cell proliferation

Abstract: GH(4)C(1) cells are a clonal strain of rat pituitary cells that synthesize and secrete prolactin and growth hormone. Chronic treatment (longer than 24 h) of GH(4)C(1) cells with epidermal growth factor (EGF) (10(-8) M) decreased by 30-40 percent both the rate of cell proliferation and the plateau density reached by cultures. Inhibition of cell proliferation was accompanied by a change in cellular morphology from a spherical appearance to an elongated flattened shape and by a 40-60 percent increase in cell volume. These actions of EGF were qualitatively similar to those of the hypothalamic tripeptide thyrotropin-releasing hormone (TRH) (10(-7) M) which decreased the rate of cell proliferation by 10-20 percent and caused a 15 percent increase in cell volume. The presence of supramaximal concentrations of both EGF (10(-8)M) and TRH (10(-7)M) resulted in greater effects on cell volume and cell multiplication than either peptide alone. EGF also altered hormone production by GH(4)C(1) cells in the same manner as TRH. Treatment of cultures with 10(-8) M EGF for 2-6 d increased prolactin synthesis five- to ninefold compared to a two- to threefold stimulation by 10(-7) M TRH. Growth hormone production by the same cultures was inhibited 40 percent by EGF and 15 percent by TRH. The half- maximal effect of EGF to increase prolactin synthesis, decrease growth hormone production, and inhibit cell proliferation occurred at a concentration of 5 x 10 (-11) M. Insulin and multiplication stimulating activity, two other growth factors tested, did not alter cell proliferation, cell morphology, or hormone production by GH(4)C(1) cells, indicating the specificity of the EGF effect. Fibroblast growth factor, however, had effects similar to those of EGF and TRH. Of five pituitary cell strains tested, all but one responded to chronic EGF treatment with specifically altered hormone production. Acute chronic EGF treatment with specifically altered hormone production. Acute treatment (30 min) of GH(4)C(1) cells with 10(-8) M EGF caused a 30 percent enhancement of prolactin release compared to a greater than twofold increase caused by 10(-7) M TRH. Therefore, although EGF and TRH have qualitatively similar effects on GH(4)C(1) cells, their powers to affect hormone release acutely or hormone synthesis and cell proliferation chronically are distinct.

Chorionic growth hormone-prolactin (cgp): secretion, disposition, biologic activity in man, and postulated function as the “growth hormone” of the second half of pregnancy*

Abstract: It is now firmly established that the human placenta synthesizes and secretes a polypeptide hormone that is chemically and immunologically similar to human pituitary growth hormone and that has prolactin-like and growth hormone-like activity (see Josimovich & Brande, 1964; Grumbach & Kaplan, 1964a & b; and Kaplan & Grumbach, 1964, for historical review and a summary of early observations). A comparable simian placental hormone was identified (Kaplan & Grumbach, 1964) that bears an even closer immunochemical relationship to the human placental hormone than either has to its respective pituitary growth hormone. Josimovich isolated this hormone and emphasized its prolactin and luteotropic activity in animals (Josimovich & MacLaren, 1962; Josimovich et at., 1963; Josimovich & Atwood, 1964) and named it “human placental lactogen.” In our early studies, we obtained data suggesting that this placental polypeptide also exhibited growth hormone-like activity on bioassay. The hypothesis was advanced that changes in carbohydrate, fat, and protein metabolism in the last half of pregnancy, previously ascribed to pituitary growth hormone, were effected, a t least in part, by the placental hormone (Grumbach & Kaplan, 1964a & b; Kaplan & Grumbach, 1964). I t was postulated that the placental polypeptide, rather than pituitary hormone, functioned as an important “metabolic hormone” of late pregnancy; the adaptive and homeostatic advantages to the mother and fetus of such a placental function were pointed out. To indicate the duality of biologic properties of the placental protein which simulated those of human pituitary growth hormone and its origin in the syncytiotrophoblast, we proposed the tentative designation human “chorionic growth hormone-prolactin” (CGP) . Subsequently, additional evidence was obtained in this laboratory to support the growth hormone-like properties of CGP in man and its metabolic role in pregnancy (Grumbach, 1965; Kaplan & Grumbach, 1965b; Grumbach et al . , 1966). *Supported by grants from the National Institute of Child Health and Human Development and the National Institute of Arthritis and Metabolic Diseases, NIH, USPHS

Alternative role for prolactin-releasing peptide in the regulation of food intake.

Abstract: Prolactin-releasing peptide (PrRP) is a peptide ligand for the human orphan G-protein-coupled receptor hGR3/GPR10 and causes the secretion of prolactin from anterior pituitary cells. However, the lack of immunoreactive staining for PrRP in the external layer of the median eminence seems to rule out this peptide as a classical hypophysiotropic hormone and, furthermore, PrRP is less effective than another inducer of prolactin secretion, thyrotropin-releasing hormone, both in vitro and in vivo. Here we show a reduction in the expression of PrRP mRNA during lactation and fasting and an acute effect of PrRP on food intake and body weight, supporting the hypothesis of an alternative role for the peptide.

Drugs Five Years Later: Bromocriptine

Abstract: Bromocriptine, a specific dopamine receptor agonist, has been used for the treatment of various hyperprolactinemic conditions and as adjunctive therapy for acromegaly (with or without concomitant hyperprolactinemia) and Parkinson's disease. Bromocriptine is extremely effective in suppressing prolactin secretion regardless of the cause, in restoring gonadal function and fertility, and in decreasing the size of prolactin-secreting pituitary tumors. Most patients with acromegaly have clinical improvement with this drug. When bromocriptine is added to a regimen of levodopa or carbidopa, patients with Parkinson's disease frequently have additional clinical improvement and, in most patients, the levodopa or carbidopa dose can be reduced. Withdrawal of bromocriptine therapy is associated in most patients with reversal of its beneficial effects--return of hyperprolactinemia, return of excess growth hormone secretion, and exacerbation of Parkinson's disease.

Uterine and placental factors regulating conceptus growth in domestic animals.

Abstract: All mammalian uteri contain endometrial glands that synthesize or transport and secrete substances essential for survival and development of the conceptus (embryo/fetus and associated extraembryonic membranes). The ovine uterine gland knockout ewe model supports a primary role for endometrial glands and, by default, their secretions as essential for conceptus survival and development during the peri-implantation period of pregnancy. Endometrial adenogenesis, the process whereby glands develop in the uterus, is primarily a postnatal event in domestic and laboratory animals, as well as in humans. Endometrial adenogenesis involves differentiation and budding of glandular epithelium from lumenal epithelium, followed by invagination and extensive tubular coiling and branching morphogenesis throughout uterine stroma to the myometrium. In sheep, pituitary prolactin acting on prolactin receptors expressed by uterine glandular epithelium regulates endometrial adenogenesis. In contrast, expression and functional activation of estrogen receptor alpha in the uterus is a primary regulator of endometrial adenogenesis in the pig. In adult sheep and pigs, extensive endometrial gland hyperplasia and hypertrophy occur during gestation, presumably to provide increasing histotrophic support for conceptus growth and development. A servomechanism has been proposed in sheep and pigs to regulate endometrial gland development and differentiated function during pregnancy that involves sequential actions of ovarian steroid hormones, pregnancy recognition signals, and lactogenic hormones from the pituitary and/or placenta. The fact that disruption of uterine development during critical organizational periods can alter the functional capacity and embryotrophic potential of the adult uterus reinforces the importance of understanding uterine developmental biology. Defects in endometrial gland morphogenesis during uterine growth and development may cause the unexplained, high rates of peri-implantation embryonic loss in domestic animals and humans. Knowledge of the basic mechanisms regulating uterine development is expected to suggest means to increase uterine capacity, litter size, and neonatal survival, as well as ameliorate certain types of infertility.