Berelowitz M, Kronheim S, Pimstone B, Shapiro B
J Clin Invest. 1978 May;61(5):1410-4. doi: 10.1172/JCI109059.
Somatostatin-like immunoreactivity (SLI) has been demonstrated by radioimmunoassay (RIA) in rat serum using an antiserum specific for somatostatin and cross-reacting maximally with the biologically important area on the peptide. The RIA has a sensitivity of 35 pg/ml. SLI dilutes in parallel with synthetic somatostatin standard in the RIA and shows characteristics similar to synthetic somatostatin on Sephadex G-25 (f) gel chromatography eluting largely as a single peak with 1 M acetic acid. Significant regional differences in serum SLI are present. A positive gradient was found in paired samples from aorta (mean+/-SEM, 0.304+/-0.024 ng/ml) and portal vein (0.495+/-0.047 ng/ml) consistent with the known presence of somatostatin in gut and pancreas, and a negative gradient was noted between paired samples from portal vein (0.523+/-0.076 ng/ml) and hepatic vein (0.290+/-0.048 ng/ml) indicating hepatic clearance. No significant differences were demonstrated between aorta and confluence of cerebral venous sinuses or between aorta and inferior vena cava (IVC). After intragastric glucose, a significant and marked elevation of portal SLI was observed, maximal at 5 min (0.416+/-0.137 vs. 1.55+/-0.30 ng/ml at 5 min). A significant biphasic elevation of portal SLI also occurred after intravenous glucose. After both routes of glucose administration, the patterns of portal SLI followed closely those of portal glucose and insulin. By contrast, IVC SLI failed to reflect these changes.Thus, SLI in the rat shows chromatographic similarity with synthetic somatostatin. Regional differences in serum levels are marked; the highest concentrations being found in the portal venous effluent of pancreas and gut. Furthermore, glucose causes elevation of portal SLI in a pattern similar to portal insulin and glucose and without concomitant elevation in IVC. This differential elevation of SLI after glucose is consistent with a hormonal action within the portal system as a direct effect of somatostatin on the liver has previously been demonstrated. In addition, the liver is important in the clearance of portal SLI, possibly to prevent extraportal effects in response to gut and pancreatic stimulation. Finally, it is clear that regional sampling of serum for SLI measurement may be critical in the investigation of the putative physiological roles for somatostatin.
使用对生长抑素具有特异性且与该肽的生物学重要区域最大程度交叉反应的抗血清，通过放射免疫分析（RIA）已在大鼠血清中证实了生长抑素样免疫反应性（SLI）。该RIA的灵敏度为35 pg/ml。在RIA中，SLI与合成生长抑素标准品呈平行稀释，并且在Sephadex G - 25（f）凝胶色谱上显示出与合成生长抑素相似的特征，主要以单峰形式被1 M乙酸洗脱。血清SLI存在显著的区域差异。在来自主动脉（均值±标准误，0.304±0.024 ng/ml）和门静脉（0.495±0.047 ng/ml）的配对样本中发现了正向梯度，这与肠道和胰腺中已知存在生长抑素一致；在来自门静脉（0.523±0.076 ng/ml）和肝静脉（0.290±0.048 ng/ml）的配对样本之间观察到负向梯度，表明肝脏有清除作用。在主动脉与脑静脉窦汇合处之间或主动脉与下腔静脉（IVC）之间未显示出显著差异。胃内给予葡萄糖后，观察到门静脉SLI显著且明显升高，在5分钟时达到峰值（0.416±0.137对5分钟时的1.55±0.30 ng/ml）。静脉注射葡萄糖后门静脉SLI也出现显著的双相升高。在两种葡萄糖给药途径后，门静脉SLI的模式与门静脉葡萄糖和胰岛素的模式密切相关。相比之下，IVC SLI未能反映这些变化。因此，大鼠体内的SLI在色谱上与合成生长抑素相似。血清水平存在区域差异；在胰腺和肠道的门静脉流出液中发现浓度最高。此外，葡萄糖导致门静脉SLI升高的模式与门静脉胰岛素和葡萄糖相似，且IVC中未伴随升高。葡萄糖后SLI的这种差异升高与门静脉系统内的激素作用一致，因为先前已证明生长抑素对肝脏有直接作用。此外，肝脏在清除门静脉SLI方面很重要，可能是为了防止对肠道和胰腺刺激产生门静脉外效应。最后，很明显，对血清进行区域采样以测量SLI对于研究生长抑素假定的生理作用可能至关重要。
