Luteinizing hormone

About: Luteinizing hormone is a research topic. Over the lifetime, 23961 publications have been published within this topic receiving 756054 citations. The topic is also known as: lutropin & glyco-Lutropin.

Estrogen Resistance Caused by a Mutation in the Estrogen-Receptor Gene in a Man

Abstract: Background and Methods Mutations in the estrogen-receptor gene have been thought to be lethal. A 28-year-old man whose estrogen resistance was caused by a disruptive mutation in the estrogen-receptor gene underwent studies of pituitary-gonadal function and bone density and received transdermal estrogen for six months. Estrogen-receptor DNA, extracted from lymphocytes, was evaluated by analysis of single-strand-conformation polymorphisms and by direct sequencing. Results The patient was tall (204 cm [80.3 in.]) and had incomplete epiphyseal closure, with a history of continued linear growth into adulthood despite otherwise normal pubertal development. He was normally masculinized and had bilateral axillary acanthosis nigricans. Serum estradiol and estrone concentrations were elevated, and serum testosterone concentrations were normal. Serum follicle-stimulating hormone and luteinizing hormone concentrations were increased. Glucose tolerance was impaired, and hyperinsulinemia was present. The bone mineral d...

The neuroendocrine control of the menstrual cycle.

Abstract: Publisher Summary This chapter discusses the construction of a model of the neuroendocrine control system that governs the 28-day ovarian cycle of the rhesus monkey. This model has three basic components: the arcuate nucleus of the hypothalamus, the gonadotrophs of the pituitary gland, and the ovary. The arcuate nucleus is the central component of the control system. The gonadotrophs respond to this unvarying pulsatile gonadotropin releasing hormone (GnRH) stimulation by releasing pulses of follicle stimulating hormone (FSH) and luteinizing hormone (LH). Immature follicles respond to this unvarying gonadotropic stimulus by increasing in size and secreting increasing quantities of estradiol, which achieve maxima near mid-cycle. This process occupies approximately 14 days. The magnitude of the response to each GnRH pulse is modulated by estradiol acting directly on the gonadotrophs. The characteristic duration of the rhesus monkey ovarian cycle is thus determined by the duration of follicular development. This can occur in the presence of an absolutely unvarying pattern of hypophysiotropic stimulation.

Purification and characterization of an FSH releasing protein from porcine ovarian follicular fluid.

Abstract: A variety of hypophysiotropic peptides or proteins have been reported to be present in mammalian gonads. Inhibin, a hormone that under most circumstances selectively suppresses the secretion of follicle-stimulating hormone (FSH) but not luteinizing hormone (LH), has been isolated from the gonadal fluids of several species1–5 and characterized as a heterodimeric protein consisting of α- and β-polypeptides associated by disulphide bonds. The complete amino-acid sequences of the precursors of porcine6,7 and human7 inhibin α-subunits and two distinct porcine inhibin β-subunits (βA and βB)6 have been deduced from complementary DNA sequences. Gonadotropin releasing peptides have also been found in the gonad and have generally been shown to be active in radioreceptor assays for gonadotropin releasing hormone (GnRH) but to exhibit different chromatographic and immunological characteristics from those of GnRH8–14. During our purification of inhibin from porcine follicular fluid, we noted fractions that could stimulate the secretion of FSH by cultured anterior pituitary cells3. We report here the purification of an FSH releasing protein (FRP) and its characterization by SDS-polyacrylamide gel electrophoresis under non-reducing and reducing conditions and by partial sequence analysis. Our results indicate that porcine gonadal FRP is a homodimer consisting of two inhibin βA-chains linked by disulphide bonds. FRP is highly potent (50% effective concentration (EC50)∼25 pM) in stimulating the secretion and biosynthesis of FSH but not of LH or any other pituitary hormone. In contrast to the effects of GnRH and other reported gonadal gonadotropin releasing fractions, the action of FRP is not mediated by GnRH receptors.

Kisspeptin directly stimulates gonadotropin-releasing hormone release via G protein-coupled receptor 54

Abstract: We have recently described a molecular gatekeeper of the hypothalamic-pituitary-gonadal axis with the observation that G protein-coupled receptor 54 (GPR54) is required in mice and men for the pubertal onset of pulsatile luteinizing hormone (LH) and follicle-stimulating hormone (FSH) secretion to occur. In the present study, we investigate the possible central mode of action of GPR54 and kisspeptin ligand. First, we show that GPR54 transcripts are colocalized with gonadotropin-releasing hormone (GnRH) neurons in the mouse hypothalamus, suggesting that kisspeptin, the GPR54 ligand, may act directly on these neurons. Next, we show that GnRH neurons seem anatomically normal in gpr54–/– mice, and that they show projections to the median eminence, which demonstrates that the hypogonadism in gpr54–/– mice is not due to an abnormal migration of GnRH neurons (as occurs with KAL1 mutations), but that it is more likely due to a lack of GnRH release or absence of GnRH neuron stimulation. We also show that levels of kisspeptin injected i.p., which stimulate robust LH and FSH release in wild-type mice, have no effect in gpr54–/– mice, and therefore that kisspeptin acts directly and uniquely by means of GPR54 signaling for this function. Finally, we demonstrate by direct measurement, that the central administration of kisspeptin intracerebroventricularly in sheep produces a dramatic release of GnRH into the cerebrospinal fluid, with a parallel rise in serum LH, demonstrating that a key action of kisspeptin on the hypothalamo-pituitary-gonadal axis occurs directly at the level of GnRH release. The localization and GnRH release effects of kisspeptin thus define GPR54 as a major control point in the reproductive axis and suggest kisspeptin to be a neurohormonal effector.