Lactogenic hormones stimulate the liver to secrete a factor that acts synergistically with prolactin to promote growth of the pigeon crop-sac mucosal epithelium in vivo.

Lactogenic hormones stimulate the liver to secrete a factor that acts synergistically with prolactin to promote growth of the pigeon crop-sac mucosal epithelium in vivo.
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催乳激素刺激肝脏分泌一种与催乳素协同作用的因子,促进体内鸽嗉囊粘膜上皮的生长。

DOI:
10.1210/endo-116-4-1449
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发表时间:
1985
期刊:
影响因子:
4.8
通讯作者:
S. Russell
S. Russell
中科院分区:
医学2区
文献类型:
--
作者:
C. S. Nicoll;N. Hebert;S. Russell

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我们研究了肝脏是否是 PRL 协同活性(即 Synlactin)的来源,并且我们获得了一些有关其分泌的内分泌控制的信息。从 3 个月大的 Long-Evans 大鼠(雄性、处女、怀孕或哺乳期雌性)或注射生理盐水、牛 GH 或羊 PRL 7 天的处女雌性中取出肝脏,并制备肝切片用于在培养基 199 中体外培养。通过确定培养基是否可以增强鸽子嗉囊对局部注射的羊 PRL 的反应来测试突触素活性。只有含有来自怀孕或哺乳期女性和注射 PRL 的处女肝脏因子的培养基才具有显着的突触乳素活性。它们分别将嗉囊粘膜生长反应增强了 130%、140% 和 103%。孵育来自处女或怀孕大鼠的肾脏切片的培养基没有可检测到的突触乳素活性。还测试了具有 Synlactin 活性的培养基样品中是否存在生物活性(作物囊测定)和免疫反应性 (RIA) 大鼠 PRL,但均未检测到该激素的含量。因此,增强作用并不是由肝脏隔离和释放的 PRL 造成的。通过 RIA 测量有或没有 Synlactin 活性(分别来自怀孕和处女女性)的培养基样品中胰岛素样生长因子 I/生长调节素-C 的水平,结果发现是相当的。因此,突乳素活性可能不是由胰岛素样生长因子 I 引起的。总体而言,我们的结果表明,催乳激素(即垂体 P​​RL,以及怀孕大鼠中可能的胎盘催乳激素)刺激肝脏分泌突乳素活性。怀孕女性体内数量增加的肝脏 PRL 受体可能参与突乳素的分泌,然后突乳素可与卵巢类固醇和 GH 和/或 PRL 协同作用,促进乳腺生长。
We have investigated whether the liver is a source of a PRL-synergizing activity (i.e. synlactin) and we have obtained some information on endocrine control of its secretion. Livers were removed from 3-month-old Long-Evans rats (male, virgin, pregnant, or lactating female) or from virgin females that were injected with saline, bovine GH, or ovine PRL for 7 days, and hepatic slices were prepared for in vitro incubation in medium 199. The media were tested for synlactin activity by determining whether they could augment the pigeon crop-sac response to locally injected ovine PRL. Only the media containing factors from the liver of pregnant or lactating females and PRL-injected virgins had significant synlactin activity. They augmented the crop-sac mucosal growth response by 130%, 140%, and 103%, respectively. Medium in which slices of kidney from virgin or pregnant rats were incubated did not have detectable synlactin activity. The medium samples that had synlactin activity were also tested for the presence of bioactive (crop-sac assay) and immunoreactive (RIA) rat PRL, and none had detectable amounts of the hormone. Hence, the augmenting effect is not due to PRL that is sequestered in and released by the liver. The levels of insulin-like growth factor I/somatomedin-C in medium samples that did or did not have synlactin activity (from pregnant and virgin females, respectively) were measured by RIA and were found to be equivalent. Hence, synlactin activity is probably not due to insulin-like growth factor I. Overall, our results indicate that lactogenic hormones (i.e. pituitary PRL, and presumably placental lactogens in the pregnant rats) stimulate the liver to secrete synlactin activity. The hepatic PRL receptors which increase in number in pregnant females may be involved in the secretion of synlactin, which could then act in concert with ovarian steroids and GH and/or PRL to promote mammary growth.
DOI: 10.1210/endo-110-2-668
发表时间: 1982
期刊: Endocrinology
影响因子: 4.8
作者:
Soares,MJ;Colosi,P;Talamantes,F
通讯作者: Talamantes,F