Stimulatory effects of ghrelin on circulating somatostatin and pancreatic polypeptide levels
Stimulatory effects of ghrelin on circulating somatostatin and pancreatic polypeptide levels
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DOI：
10.1210/jc.2002-021161
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发表时间：
2003-02-01
影响因子：
5.8
通讯作者：
Peracchi, M
中科院分区：
文献类型：
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作者：
Arosio, M;Ronchi, CL;Peracchi, M
Ghrelin是最近发现的GH促分泌素受体的内源性配体，是一种具有内分泌、食欲和胃肠道作用的肠脑肽。在啮齿类动物中，它增加循环胃泌素和胰岛素水平，而在人类中，尽管血糖水平升高，但它似乎减少胰岛素分泌。本研究的目的是评估生长激素释放肽管理对总循环生长抑素（SS），胰多肽（PP）和胃泌素水平的影响，与胰岛素，葡萄糖和GH引起的。八名正常体重的健康志愿者（四名女性和四名男性）在两个不同的日子禁食过夜后注射3.3 μ g/kg的生长素释放肽或生理盐水。每15分钟采血一次，持续1小时，然后每30分钟采血一次，持续2小时。正如预期的那样，生长激素释放肽注射引起迅速GH和葡萄糖增加，在30分钟达到峰值，胰岛素减少，在60分钟达到最低点。胃泌素浓度没有改变，而SS（在15和120分钟达到峰值的双相模式）和PP（迅速增加，在15分钟达到峰值）均观察到显著升高。SS第一峰与胰岛素变化呈显著负相关（r = -0.86; P < 0.01）。总之，这项研究清楚地表明，ghrelin刺激SS和PP释放在man. Although这些药理作用的潜在机制和生物学意义仍有待阐明，SS增加和胰岛素变化之间的因果关系可以假设。最后，这些发现强烈支持生长激素释放肽的假定作用，连接能量平衡和生长的内分泌控制与胃肠功能的调节。
Ghrelin, the recently identified endogenous ligand of the GH secretagogue receptor, is a gut-brain peptide with endocrine, orexigenic, and gastrointestinal effects. In rodents it increases circulating gastrin and insulin levels, whereas in man it appears to decrease insulin secretion despite a rise in blood glucose levels. The aim of the present study was to evaluate the effects of ghrelin administration on total circulating somatostatin (SS), pancreatic polypeptide (PP); and gastrin levels compared with those elicited on insulin, glucose, and GH. Eight healthy volunteers of normal weight (four women and four men) were injected with 3.3 mug/kg ghrelin or saline after an overnight fast on 2 different days. Blood was taken every 15 min for 1 h and then every 30 min for 2 h. As expected, ghrelin injection elicited a prompt GH and glucose increase with a peak at 30 min and an insulin decrease with a nadir at 60 min. Gastrin concentrations were not modified, whereas significant rises were observed in both SS (in a biphasic pattern with peaks at 15 and 120 min) and PP (which increased promptly with a peak at 15 min). A significant negative correlation was found between SS (first peak) and insulin changes (r = -0.86; P < 0.01). In conclusion, this study clearly demonstrates that ghrelin stimulates SS and PP release in man. Although the underlying mechanisms and biological significance of these pharmacological effects remain to be elucidated, a causal relationship between the SS increase and the insulin changes may be hypothesized. Finally, these findings strongly support ghrelin's postulated role in linking the endocrine control of energy balance and growth with the regulation of gastrointestinal functions.