Wilson P A, Melmed R N, Hampe M M, Holt S J
Gut. 1978 Apr;19(4):260-6. doi: 10.1136/gut.19.4.260.
To investigate further the cause of the pancreatic enlargment induced by orally ingested soybean trypsin inhibitor (STI), antibodies raised against STI and purified by affinity chromatography were used to localise dietary STI in the rat gut by fluorescent immunocytochemical methods. This technique permitted the clear intracellular demonstration of STI in the ileal mucosa of suckling rats. However, in adult rats no entry of STI into mucosal cells of the small intestine could be demonstrated, it being confined to the luminal surface of the mucosa. Although the passage of STI into and across the adult intestinal mucosa could not be excluded through the use of this technique, the results are consistent with an intraluminal mode of action of STI as suggested by Green and Lyman (1972)--namely, that the pancreatic enlargement caused in sensitive species results from the inhibition of trypsin (which acts as the physiological inhibitor of the mucosal secretion of pancreotrophic hormones), thus resulting in the uninhibited secretion of these hormones.
为了进一步研究口服大豆胰蛋白酶抑制剂（STI）导致胰腺肿大的原因，通过亲和层析法制备并纯化了抗STI抗体，采用荧光免疫细胞化学方法在大鼠肠道中定位膳食中的STI。该技术能够清晰地在哺乳大鼠回肠黏膜细胞内显示STI的存在。然而，在成年大鼠中，未发现STI进入小肠黏膜细胞，它仅局限于黏膜的管腔表面。尽管使用该技术不能排除STI进入并穿过成年大鼠肠黏膜的可能性，但这些结果与Green和Lyman（1972年）提出的STI腔内作用模式一致，即敏感物种中胰腺肿大是由于胰蛋白酶（作为胰腺营养激素黏膜分泌的生理抑制剂）受到抑制，从而导致这些激素不受抑制地分泌。
