The release of rat intestinal cholecystokinin after oral trypsin inhibitor measured by bio‐assay.
The release of rat intestinal cholecystokinin after oral trypsin inhibitor measured by bio‐assay.
复制标题
生物测定法测定口服胰蛋白酶抑制剂后大鼠肠道缩胆囊素的释放。
DOI:
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发表时间:
1981
期刊:
影响因子:
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通讯作者:
R. G. Morgan
中科院分区:
文献类型:
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作者:
S. Brand;R. G. Morgan
The distribution, molecular form and release of cholecystokinin (CCK)‐like activity in extracts of rat small intestine was studied with an in vitro gall‐bladder bio‐assay. In contrast to the reported heterogeneity of CCK‐like immunoreactivity in the intestine, only a single molecular form of CCK‐like activity was detected using the bio‐assay. 2. The CCK‐like activity eluted from Sephadex G50 with a Kav of 0.69, after the triacontriapeptide of cholecystokinin (CCK33) and before cholecystokinin octapeptide 2500, may represent the 22 amino acid peptide of CCK (CCK22). The bio‐assay peak of CCK‐like activity had pancreozymin activity and CCK/gastrin C terminal immunoreactivity. The CCK‐like activity weas readily extracted from the small intestine at neutral pH, but subsequent treatment with cold 0.5 M‐acetic acid extracted further CCK‐like activity of the same molecular form as that recovered under neutral conditions. 3. The bio‐assay detected no CCK‐like activity, nor was pancreozymin‐like activity found in fractions corresponding to CCK33 or CCK8 after Sephadex G50 chromatography of rat intestinal extracts. 4. Oral trypsin inhibitor was a potent stimulus for the release of CCK‐like activity from the upper small intestine of the rat. After oral trypsin inhibitor release, CCK‐like activity was rapidly resynthesized.