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Prolactin in humans

Muller H, Hiemke C, Hammes E, Hess G. Sub-acute effects of interferon-alpha 2 on adrenocorticotrophic hormone, cortisol, growth hormone and prolactin in humans. Psychoneuroendocrinology 1992 17(5) 459-65. [Pg.671]

Dietary Fat, Prolactin, and Breast Cancer. Prolactin may also interact with diet to influence breast cancer. Although the role of prolactin in human breast cancer etiology is relatively obscure, its role as a promotor in rodent mammary carcinogenesis has been well established (55,56). [Pg.317]

Dogusan Z, Hooghe R, Verdood P, Hooghe-Peters EL Cytokine-like effects of prolactin in human mononuclear and polymorphonuclear leukocytes. J Neuroimmunol 2001 120 58-66. [Pg.20]

A hypersecretion of the hormone is generally implicated in the pathogenesis of the polypeptide-hormone-derived amyloids (Westermark 1994). The pituitary gland can maintain a prolactin secretory capacity at old age (Rolandi et al. 1982), and age per se does not seem to alter the rate of secretion of prolactin in humans (Yamaji et al. 1976), nor is the circadian rhythms of prolactin plasma levels modified at old age (Touitou et al. 1981). [Pg.675]

Takahara J, Yunoki S, Yakushiji W, et ah Stimulatory effects of gamma-hydroxybutyric acid on growth hormone and prolactin release in humans. J Clin Endocrinol Metab 44 1014-1017, 1977... [Pg.267]

There is a recent clinical report by Emil Coeearo and colleagues that I think might be relevant to the kind of thing you have done in rats. They have been looking at endocrine responses to fenfluramine in humans as a marker of central serotonergic function. And they have observed an increase in serum prolactin concentration, which is felt to be due to serotonin release. They reported that, in subjects who received a seeond dose of fenfluramine within 12 days after the first dose, that there was a blunted response to serum prolactin. [Pg.155]

If PCP produces its multitude of effects by activating PCP (sigma) receptors, then chronic exposure to agonists should elicit the development of tolerance. Tolerance to plasma prolactin suppression by PCP is observed in rats following daily administration for 28 days (Quirion et al. 1982). Chronic PCP treatment has been also shown to reduce the number of PCP sites (receptors) in rodent brains (Quiriun et al. 1983). Behavioral studies have documented the development of tolerance to and dependence on PCP (Balster and Woolverton 1980 Flint and Ho 1980). A tolerance syndrome develops in humans, in which the user is compelled to increase his intake of drug (Jain et al. 1977). [Pg.143]

Neuroendocrine effects DMT causes a transient increase in release of several hormones. In humans intravenously administered DMT (0.4 mg/kg), increases are seen in j8-endorphin, corticotrophin, prolactin, cor-... [Pg.368]

Armario A, Marti 0, Molina T, de Pablo J, Valdes M. (1996). Acute stress markers in humans response of plasma glucose, cortisol, and prolactin to two examinations differing in the anxiety they provoke. Psychoneuroendocrinology. 21(1) 17-24. [Pg.503]

D5 has slightly different properties than D4, and it does not have any estrogenic activity [289]. It does, however, also have adverse effects on the reproductive system, much like D4, but also on the adipose tissue, bile production, and even immune system due to D5 s effect of reducing the prolactin levels [291]. In addition, it was determined that D5 causes a significant increase in uterine tumors in rats after a 160 ppm exposure. However, it is proposed that the tumors occur in rats through a mechanism that would not affect humans [291]. D5 also acts as a dopamine agonist and it can cause adverse effects on the nervous system in humans [291]. For exposures to D6 in rats, an increase in liver and thyroid mass and reproductive effects were observed [292]. [Pg.287]

Whereas several peptides besides AVP are known to act synergistically with CRH, the only peptide candidate in humans that inhibits the HPA system at all regulatory levels of the system seems to be atrial natriuretic peptide (ANP). ANP has been shown to inhibit the stimulated release of CRH and ACTH in vitro and in vivo. This could be observed in humans as well, where ANP inhibits the CRH-induced ACTH (Keller et al. 1992), prolactin (Wiedemann et al. 1995), and cortisol secretion (StrOhle et al. 1998). ANP is not only synthesized by atrial myocytes (deBold et al. 1985) and released into the circulation, but is also found in neurons of different brain regions (Tanala et al. 1984) where specific receptors have been found. ANP receptors and immunoreactivity have been found in periventricular and paraventricular hypothalamic nuclei, the LC, and the central nucleus of the amygdala. [Pg.511]

Ellingboe. Acute effects of marihuana smoking on prolactin levels in human females. J Pharmacol Exp Ther 1985 232(1) 220-222. [Pg.103]

All azapirones increase the turnover of both cerebral dopamine and norepinephrin. At high doses they cause a mild elevation of prolactin (Baldessarini, 1996). However, in humans, doses of 30 mg/day for 28 days led to no changes in the levels of prolactin, growth hormone, or cortisol (Jann, 1988)... [Pg.346]

Endocrine system Dopamine inhibits prolactin release in human being. It also acts on somatotrophs to increase growth hormone release. [Pg.124]

Limited data were available to evaluate the toxic effects of ethylbenzene in humans. Liver and kidney weights were increased in rats following exposure to ethylbenzene with no signs of hepatic necrosis. Cytochrome P450 enzymes were induced in both liver and kidney of ethylbenzene-exposed rats. Ethylbenzene caused changes in dopamine levels in brain and prolactin secretion in rats exposed for three to seven days. In rat brain cell cultures, ethylbenzene decreased the activity of several integral membrane enz5unes. [Pg.256]

Growth hormone is a 191-amino-acid peptide with two sulfhydryl bridges. Its structure closely resembles that of prolactin. In the past, medicinal GH was isolated from the pituitaries of human cadavers. However, this form of GH was found to be contaminated with prions that could cause Creutzfeldt-Jakob disease. For this reason, it is no longer used. Somatropin, the recombinant form of GH, has a 191-amino acid sequence that is identical with the predominant native form of human GH. [Pg.827]

Thyroid Effects. Limited information is available on thyroid effects in PBDE-exposed humans. There are suggestive occupational data as shown by effects that included increased serum FSH, low or borderline low serum T4, and increased thyroid antimicrosomal antibody titers in workers exposed to decaBDE and/or unspecified PBBs. There was no clear association between plasma levels of 2,2, 4,4-tetraBDE and thyroid hormone levels (free and total T3 and T4, TSH, free testosterone, follicle-stimulating hormone, lutenizing hormone, and prolactin) in men who consumed varying amounts of fatty fish from the Baltic Sea. Based on consistent evidence in animals, as summarized below, the thyroid is particularly sensitive to PBDEs and is a likely target of toxicity in exposed humans. [Pg.42]

Studies in humans have suggested that serum prolactin may be lower on vegetarian-low fat diets (57,58). As previously noted for serum estrogen, studies in laboratory animals have shown inconsistent effects. Some studies report elevations of serum prolactin with high fat diets (51,59,60) whereas others show no change... [Pg.317]


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See also in sourсe #XX -- [ Pg.99 ]




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Prolactin

Prolactin humans

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