Growth hormone increases somatostatin release and messenger ribonucleic acid levels in the rat hypothalamus.
Growth hormone increases somatostatin release and messenger ribonucleic acid levels in the rat hypothalamus.
复制标题
生长激素增加大鼠下丘脑中生长抑素的释放和信使核糖核酸水平。
DOI：
10.1016/0006-8993(93)90014-e
复制
发表时间：
1993
期刊：
影响因子：
2.9
通讯作者：
McCann,SM
中科院分区：
文献类型：
--
作者：
Aguila,MC;McCann,SM
生长激素（GH）通过刺激生长抑素（SRIF）的释放来抑制其自身的分泌。因此，在离体雄性大鼠下丘脑中研究了GH释放因子（GRF）和SRIF释放以及SRIF信使核糖核酸（mRNA）的可能调节。将正中隆起（ME's）在含有10−7-10− 11 M GH的缓冲液中孵育30 min。通过RIA定量释放到培养基中的SRIF和GRF。10− 9 M GH显著增加ME碎片中SRIF的释放（P < 0.001）;然而，10− 9 M GH也抑制ME中GRF的释放（P < 0.01）。为了确定GH对SRIF mRNA水平的影响，将室周核（PeN）外植体在含有10−7-10− 11 M GH的培养基中培养6 h。在10−10-10− 7 M GH存在下，SRIF mRNA水平（通过S1核酸酶保护试验测定）显著升高。同样，10− 9 M GH在30 min和6 h显著刺激了PeN外植体的SRIF释放。令人惊讶的是，10 - 9 M GH也显著增加了这些时间点PeN外植体的GRF释放。该GRF不是GH诱导的SRIF释放或SRIF mRNA增加的原因，因为GRF抗体未改变GH诱导的SRIF释放和mRNA水平增加。这些结果表明，在ME通过抑制GRF和刺激SRIF释放介导的GH的负短环反馈，而在PeN GH增加SRIF释放和SRIF mRNA水平。生长激素诱导的增加GRF释放的PeN外植体仍然无法解释。
Growth hormone (GH) suppresses its own secretion by stimulating somatostatin (SRIF) release. Thus, the possible regulation of GH-releasing factor (GRF) and SRIF release and SRIF messenger ribonucleic acid (mRNA) by GH was studied in the hypothalamus of male rats in vitro. The median eminences (ME's) were incubated in buffer containing 10−7–10−11M GH for 30 min. SRIF and GRF released into the medium were quantitated by RIA. The release of SRIF from ME fragments was significantly increased (P < 0.001) by 10−9M GH; however, 10−9M GH also inhibited (P < 0.01) GRF release from the ME. To determine the effect of GH on SRIF mRNA levels, periventricular nucleus (PeN) explants were cultured during 6 h in medium with 10−7–10−11M GH. Levels of SRIF mRNA (determined by an S1nuclease protection assay) were significantly elevated in the presence of 10−10–10−7M GH. Likewise, 10−9M GH significantly stimulated SRIF release from PeN explants at 30 min and at 6 h. Surprisingly, 10−9M GH also significantly increased GRF release from the PeN explants at these times as well. This GRF was not responsible for the increased SRIF release or SRIF mRNA induced by GH since GRF antibody did not modify the GH-induced increases in SRIF release and mRNA levels. These results demonstrate a negative short-loop feedback of GH mediated at the ME by suppression of GRF and stimulation of SRIF release, whereas in the PeN GH increased both SRIF release and SRIF mRNA levels. The GH-induced increase in GRF release by PeN explants remains unexplained.