Enterostatin efflux in cat intestinal lymph: relation to lymph flow, hyaluronan, and fat absorption.
Enterostatin efflux in cat intestinal lymph: relation to lymph flow, hyaluronan, and fat absorption.
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猫肠道淋巴液中肠抑素的流出：与淋巴液流、透明质酸和脂肪吸收的关系。
DOI：
10.1152/ajpgi.1996.271.4.g714
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Reed,RK
中科院分区：
文献类型：
--
作者：
Townsley,MI;Erlanson-Albertsson,C;Ohlsson,A;Rippe,C;Reed,RK
这项研究中提出的问题是，胰腺前磷脂酶活化肽Enterostatin是否通过淋巴调节肠道透明质酸的周转。在麻醉猫中，通过手术从近端和远端肠道分离回肠段，插入引流淋巴管，并在原位进行自体灌流。在几个组中，比较了基线和增加淋巴流量以及没有和有脂肪吸收时淋巴中免疫活性肠抑素的浓度与血浆中的浓度。在不吸收脂肪的情况下，肠淋巴抑制素与血浆淋巴抑素的基线比值(L/P)为1.44+/-0.29，而喂奶油后为4.93+/-0.42(P<；0.05)。在另一组中，当肠腔内灌流油酸和牛磺胆酸盐的混合物2小时时，肠抑素L/P比基线增加一倍。在高淋巴流量时，所有组的肠抑素浓度都下降，导致L/P在没有脂肪吸收的情况下为0.47+/-0.09(P<；0.05)，在油酸后为0.77+/-0.35，在奶油喂养组为1.26+/-0.13。这些变化与脂肪吸收后透明质酸从回肠流出到淋巴的模式有关[R.K.Reed，M.I.Townsley，V.H.Pitts，T.C.Laurent和A.E.Taylor。上午好。J.Physiol，263(胃肠测试)肝脏生理素。26)：G6-G11,1992]然而，在不同的组中，当肠抑素以动脉闭合推注或通过肠腔注入回肠时，透明质酸从肠到淋巴的流出没有结果改变。总而言之，尽管在该模型中胰腺外分泌物向回肠腔的输送被阻断，但在脂肪吸收后，淋巴中的肠抑素浓度增加。尽管如此，似乎很清楚的是，肠抑素不会改变肠道透明质酸的周转。
The question addressed in this study was whether enterostatin, the pancreatic procolipase activation peptide, modulates intestinal hyaluronan turnover via lymph. In anesthetized cats, segments of ileum were surgically isolated from the proximal and distal gut, the draining lymphatic was cannulated, and the segment was autoperfused in situ. In several groups, concentrations of immunoreactive enterostatin in lymph were compared with that in plasma at baseline and elevated lymph flow and in the absence and presence of fat absorption. The baseline ratio of lymph enterostatin to that in plasma (L/P) in the absence of fat absorption was 1.44 +/- 0.29 compared with 4.93 +/- 0.42 after cream feeding (P < 0.05). In a separate group, when the intestinal lumen was perfused for 2 h with a mixture of oleic acid and taurocholate, enterostatin L/P doubled compared with baseline. At high lymph flows, enterostatin concentrations fell in all groups, resulting in an L/P of 0.47 +/- 0.09 (P < 0.05) in the absence of fat absorption, 0.77 +/- 0.35 after oleic acid, and 1.26 +/- 0.13 in the cream-fed group. These changes correlate with the pattern of hyaluronan efflux from the ileum into lymph after fat absorption [R.K. Reed, M.I Townsley, V.H. Pitts, T.C. Laurent, and A.E. Taylor. Am. J. Physiol, 263 (Gastrointest. Liver Physiol. 26): G6-G11, 1992] However, in separate groups when enterostatin was introduced into ileum, either as a close intra-arterial bolus or via the intestinal lumen, there were no resultant changes in efflux of hyaluronan from the intestine into lymph. In conclusion, despite the fact that delivery of pancreatic exocrine secretions to the ileal lumen was blocked in this model, enterostatin concentration in lymph increased after fat absorption. Nonetheless, it seems clear that enterostatin does not modify intestinal hyaluronan turnover.