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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,.


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Journal ArticleDOI
27 Jul 1984-JAMA
TL;DR: The mean levels of total and nonspecifically bound testosterone as well as prolactin were significantly lower than in controls, although levels remained within the physiological range.
Abstract: To investigate whether endurance running in men produced basal hormonal changes similar to those reported in women, we obtained blood samples from 31 men running at least 64 km each week and 18 sedentary controls for measurement of levels of total testosterone, non-sex hormone-binding globulin-bound and free testosterone, luteinizing hormone, follicle-stimulating hormone, prolactin, and cortisol. The mean levels of total and nonspecifically bound testosterone as well as prolactin were significantly lower than in controls, although levels remained within the physiological range. Other hormone levels were similar in both groups. The lowered testosterone and prolactin levels parallel the changes reported in women runners. (JAMA1984;252:514-516)

259 citations

Journal ArticleDOI
TL;DR: The known and speculative issues underlying the effects of the prolactin, growth hormone and placental lactogen family of proteins on angiogenesis are summarized, and important remaining enigmas in this field of research are addressed.
Abstract: Prolactin, growth hormone and placental lactogen are members of a family of polypeptide hormones which share structural similarities and biological activities. Numerous functions have been attributed to these hormones, among which stand out their recently discovered effects on angiogenesis, the process by which new blood vessels are formed from the pre-existing microvasculature. Prolactin, growth hormone and placental lactogen, along with two non-classical members of the family, proliferin and proliferin-related protein, can act both as circulating hormones and as paracrine/autocrine factors to either stimulate or inhibit various stages of the formation and remodeling of new blood vessels, including endothelial cell proliferation, migration, protease production and apoptosis. Such opposing actions can reside in similar but independent molecules, as is the case of proliferin and proliferin-related protein, which stimulate and inhibit angiogenesis respectively. The potential to exert opposing effects on angiogenesis can also reside within the same molecule as the parent protein can promote angiogenesis (i.e. prolactin, growth hormone and placental lactogen), but after proteolytic processing the resulting peptide fragment acquires anti-angiogenic properties (i.e. 16 kDa prolactin, 16 kDa growth hormone and 16 kDa placental lactogen). The unique properties of the peptide fragments versus the full-length molecules, the regulation of the protease responsible for specific protein cleavage, the selective expression of specific receptors and their associated signal transduction pathways are issues that are being investigated to further establish the precise contribution of these hormones to angiogenesis under both physiological and pathological situations. In this review article, we summarize the known and speculative issues underlying the effects of the prolactin, growth hormone and placental lactogen family of proteins on angiogenesis, and address important remaining enigmas in this field of research.

259 citations

Journal ArticleDOI
TL;DR: The effects of thyrotropin-releasing hormone (TRH) on the release of growth hormone (GH), prolactin (PRL) and thyrotopin (TSH) were investigated in patients with depression, suggesting disorders in the hypothalamo-pituitary function in depression.
Abstract: The effects of thyrotropin-releasing hormone (TRH) on the release of growth hormone (GH), prolactin (PRL) and thyrotropin (TSH) were investigated in patients with depression. Intravenous injection of synthetic TRH (500 μ) caused a significant increase in plasma GH (peak value: 7.7–35.0 ng/ml) in 8 of 13 patients with mental depression. After clinical recovery these patients had no response of plasma GH to TRH. TRH administration did not raise plasma GH in normal subjects examined. Plasma PRL responses to TRH were significantly enhanced (P < 0.05) in depressed patients compared with control subjects. Plasma TSH responses to TRH were significantly blunted in patients with depression (P < 0.05). These results suggest disorders in the hypothalamo-pituitary function in depression.

258 citations

Journal ArticleDOI
04 Apr 1975-Science
TL;DR: The observations suggest that prolactin induces its own receptor, and the increased receptor level in hypophysectomized males with a renal pituitary implant was preceded by a sustained elevation of circulating Prolactin.
Abstract: A prolactin receptor, present in adult female rat liver, can be induced in males by estrogen. Hypophysectomy diminished receptor levels in the female and rendered males unresponsive to estrogen. A renal pituitary implant blunted the decrease in hypophysectomized females and induced the receptor in hyophysectomized males. The increased receptor level in hypophysectomized males with a renal pituitary implant was preceded by a sustained elevation of circulating prolactin. Our observations suggest that prolactin induces its own receptor.

257 citations

Journal ArticleDOI
TL;DR: Normal male rats were subjected to a variety of stress stimuli including simple handling, transfer from room to room, ether anesthesia alone or combined with bleeding, and the injection of saline or epinep.
Abstract: Normal male rats were subjected to a variety of stress stimuliincluding simple handling, transfer from room to room, ether anesthesia alone or combined with bleeding, the injection of saline or epinep

256 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
2023360
2022585
2021202
2020221
2019180
2018172