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71.
72.
I. García-Tornadú G. Díaz-Torga G.S. Risso P. Silveyra N. Cataldi M.C. Ramirez M.J. Low C. Libertun D. Becu-Villalobos 《Neuropeptides》2009,43(4):267-274
In 5-month-old male and female dopamine receptor 2 (D2R) knockout mice food intake per animal was unaltered while food per g BW was increased. We wished to evaluate the effect of D2R disruption on different components of energy balance and food intake regulation. We determined hypothalamic orexin precursor (PPO) expression, its receptor OX1, serum leptin levels, hypothalamic leptin receptor (OBR), circulating and pituitary α MSH levels, as well as central MC3 and MC4 receptors and NPY mRNA in wildtype and D2R knockout mice (KO).Loss of D2R caused a marked increase in serum prolactin levels, to higher levels in females compared to male KO mice. On the other hand, it produced a female-specific increase in circulating αMSH, and hypothalamic αMSH content, while neurointermediate αMSH content was decreased in both sexes. No differences were found in hypothalamic NPY, MC3R or MC4R concentration. Hypothalamic PPO mRNA expression was significantly decreased only in female KOs, while OX1 mRNA was not different between genotypes. Serum leptin levels were also similar in both genotypes.Our results show that in female and not in male mice disruption of the D2R produces two potentially anorexigenic events: an increase in serum and hypothalamic αMSH, and a decrease in hypothalamic orexin expression. Very high prolactin levels, which are orexigenic, probably counterbalance these effects, so that food intake is slightly altered. In males, on the other hand, hypothalamic PPO, and serum or hypothalamic αMSH are not modified, and increased prolactin levels may account for increased food intake per g BW. These results suggest a sexually dimorphic participation of the D2R in food intake regulation. 相似文献
73.
Escitalopram is one of the most popular selective serotonin reuptake inhibitors (SSRIs) in current use as a first-line treatment for depression. Escitalopram is well-tolerated and rarely associated with serious side effects. Endocrine and reproductive side effects of serotonergic antidepressants are uncommon and galactorrhea is very rarely mentioned among SSRI-related side effects. Serotonin-enhancing antidepressants may result in a rise in prolactin levels through suppression of dopamine neurotransmission. In the present study, we report a case of hyperprolactinemic galactorrhea associated with escitalopram. A 36-year-old woman developed galactorrhea after initiation of escitalopram for depression and was found to have an elevated prolactin level. Escitalopram was discontinued with resolution of the patient''s galactorrhea and normalization of her prolactin level. 相似文献
74.
研究口腔鳞癌患者血清催乳素(PRL)水平的变化.采用RIA检测了79名健康者和68例口腔鳞癌患者血清PRL水平.结果表明有38.2%(26/68)的患者血清PRL水平明显升高(P<0.01);男女患者、各病变部位血清PRL水平之间无显著差异(P>0.05).提示有部分口腔鳞癌患者存在高PRL血症且可能成为口腔鳞癌一个独立的预后因素. 相似文献
75.
Endogenous plasma prolactin and baseline corticosterone concentrations were measured in Dark-eyed Juncos (Junco hyemalis, n=27) photostimulated into migratory condition to look at how these hormones may be linked to the development of migratory condition. In addition to the commonly used assay for corticosterone, a recombinant-derived European starling prolactin assay validated for Dark-eyed juncos was used to measure endogenous prolactin in order to detect small but significant changes in plasma prolactin levels. In response to transfer from short (10.5L:13.5D) to long (18L:6D) days, the birds increased in body mass, fat score, daily food intake, and nocturnal migratory locomotor activity (Zugunruhe). On short-days, both hormones were low (corticosterone mean=2.89ng/mL+/-0.48 SE; prolactin mean=6.43ng/mL+/-1.31 SE). But, within 14 days of photostimulation both hormones increased significantly (Day 14: corticosterone mean=5.71ng/mL+/-0.77 SE; prolactin mean=19.67ng/mL+/-2.81 SE), rising further by Day 48 (corticosterone mean=8.41ng/mL+/-0.72; prolactin mean=112.67ng/mL+/-9.18 SE). On Day 48, birds with the most fat (fat score=3) had significantly higher corticosterone levels than those with less fat (fat score=2). This pattern, albeit not statistically significant, was similar for prolactin. These results illustrate that, independent of the seasonal peak in prolactin associated with the onset of photorefractoriness, plasma prolactin levels can rise, in concert with corticosterone, as birds come into spring migratory condition, providing some support for earlier hypotheses that these two hormones play an integral role in the development of migratory condition. Whether similar changes in plasma prolactin occur with respect to autumn migration, as does baseline corticosterone, has yet to be determined. 相似文献
76.
77.
The Prolactin-releasing Peptide (PrRP) is a 31-aminoacid peptide produced and secreted from the hypothalamus, and postulated
to promote the prolactin release from the pituitary. However, the action of PrRP remain controversial, since it was described
to have potency comparable enough to TRH, although there are many evidences that PrRP is less potent than TRH. Here we have
studied the effects of PrRP alone or in combination with TRH in the prolactin levels of rat pituitary primary cell cultures
in vitro and also in vivo prolactin responses in randomly cycling and estrogens-treated female rats. PrRP itself increased
prolactin levels in vitro and in vivo, although in a magnitude several times lower than TRH. In vivo PrRP promotes an atypical
non-peaking progressive and maintained prolactin increase. On the other hand, PrRP markedly increased the prolactin responses
to TRH in vitro (10–30 fold increase) and in vivo (up to three-fold increase). In addition, FGF-2 and EGF, two important growth
factors present in the pituitary, reduced the PrRP-induced prolactin increase in vitro. Taken together our results suggest
that PrRP released from the hypothalamus may be relevant to modulate the circulating prolactin levels in the rat. 相似文献
78.
Prolactin-releasing peptide and its homolog RFRP-1 act in hypothalamus but not in anterior pituitary gland to stimulate stress hormone secretion 总被引:3,自引:0,他引:3
The RF-amide peptides (RFRPs), including prolactin (PRL)-releasing peptide-31 (PrRP-31) and RFRP-1, have been reported to
stimulate stress hormone secretion by either direct pituitary or indirect hypothalamic actions. We examined the possible direct
effects of these peptides on PRL and adrenocorticotropin (adrenocorticotropic hormone [ACTH]) release from dispersed anterior
pituitary cells in culture and on PRL and ACTH secretion following intracerebroventricular (icv) administration in vivo. Neither
peptide significantly altered PRL or ACTH release from cultured pituitary cells (male rat donors). Central administration
of 1.0 and 3.0 nmol of PrRP-31, but only the higher dose of RFRP-1, significantly elevated serum corticosterone levels in
conscious male rats. The effect of PrRP-31 was not blocked by pretreatment (iv) with the corticotropin-releasing hormone (CRH)
antagonist, α-helical CRH 9–41; however, pretreatment of the animals (iv) with an antiserum to CRH significantly lowered the
hypothalamic-pituitary-adrenal axis response to central administration of PrRP-31. On the other hand, the release of PRL was
significantly elevated by 3.0 nmol of RFRP-1, but not PrRP-31, in similarly treated, conscious male rats. Pretreatment with
the catecholamine synthesis inhibitor, α-methyl-para-tyrosine, prevented the stimulation of PRL secretion observed following
central administration of RFRP-1. RFRP-1 similarly did not alter PRL secretion in rats pretreated with the dopamine, D2 receptor blocker, domperidone. These results suggest that the RF-amide peptides are not true neuroendocrine regulators of
stress hormone secretion in the rat but, instead, act centrally to alter the release of neuroendocrine factors that do act
in the pituitary gland to control PRL and ACTH release. In the case of RFRP-1, stimulation of PRL secretion is potentially
owing to an action of the peptide to inhibit dopamine release into the median eminence. The corticosterone secretion observed
following central administration of PrRP-31 does not appear, based on our current results, to be solely owing to an action
of the peptide on CRH-producing neurons but, instead, may be a result of the ability of PrRP-31 to increase as well the exposure
of the corticotrophs in vivo to other ACTH secretagogues, such as oxytocin or vasopressin. 相似文献
79.
The physiological effects of ovine prolactin (oPRL) and recombinant rainbow trout prolactin (rbtPRL) on cultured gill epithelia derived from freshwater rainbow trout were assessed. Epithelia composed of either pavement cells only (single seeded inserts, SSI) or both pavement and mitochondria-rich cells (double seeded inserts, DSI) were cultured in media, supplemented with doses of oPRL ranging from 10 to 100 ng/ml. Under symmetrical culture conditions (L15 media apical/L15 media basolateral), oPRL had no effect on transepithelial resistance, paracellular permeability (assessed with PEG-4000), or Na(+) and Cl(-) transport across both preparations of cultured gill epithelia. Under asymmetrical conditions (freshwater apical/L15 media basolateral), SSI epithelia treated with oPRL (10 and 50 ng/ml), in comparison to comparably treated epithelia receiving no oPRL, exhibited a greater increase in the transepithelial resistance, particularly during the first 12h of freshwater exposure, no difference in paracellular permeability and Na(+)-K(+)-ATPase activity, and lowered net Na(+) flux rates (i.e., reduced basolateral to apical loss rates). These reflected reduced unidirectional efflux rates. The PRL effect appeared to be mainly a reduction in transcellular permeability. SSI epithelia treated with rbtPRL (10 ng/ml) exhibited similar patterns of response to those treated with oPRL. Na(+)-K(+)-ATPase activity increased in DSI epithelia treated with oPRL; however, oPRL did not stimulate ion uptake across either SSI or DSI epithelial preparations. The data demonstrated that, as the sole hormone supplement for cultured gill epithelia, PRL did not promote active ion uptake. However, the observed PRL-induced alterations in cultured gill epithelial physiology were consistent with the in vivo actions of PRL on the gills of freshwater teleost fish. 相似文献
80.
Evaluation of pituitary function is essential before pituitary surgery. In hyperprolactinaemic patients with a pituitary macrolesion,
tumoral secretion of prolactin must be distinguished from ‘disconnection’ hyperprolactinaemia; serum prolactin >200 mcg/l
is virtually diagnostic of a macroprolactinoma whereas levels <80 mcg/l usually indicate ‘disconnection’. The prolactin ‘hook
effect’ should be excluded. A minimum set of pre-operative endocrine tests should include serum electrolytes, cortisol (at
08.00–09.00 h), free-T4, TSH, prolactin, oestradiol/testosterone, LH, FSH and IGF-1. Some clinicians will choose to perform
pre-operative Synacthen or insulin tolerance testing to further define ACTH reserve. If basal cortisol, Synacthen or insulin
tolerance test results are abnormal, steroid supplementation is indicated for at least the first 48 h after surgery. If pre-operative
basal cortisol is <100 nmol/l, replacement steroids should be continued until the time of post-operative pituitary function
testing (6–8 weeks after surgery). In patients with pre-operative basal cortisol >450 nmol/l, peri-operative glucocorticoid
replacement is unnecessary and further cortisol levels should be checked a few days after surgery. Most clinicians defer detailed
evaluation of growth hormone reserve until after surgery. Diabetes insipidus is rarely a problem before surgery in patients
with pituitary adenomas but may occur post-operatively. Close co-operation between anesthetic, endocrine and surgical teams
is strongly recommended. 相似文献