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胆汁酸代谢异常是否会导致坏死性小肠结肠炎?

Does abnormal bile acid metabolism contribute to NEC?

作者信息

Halpern Melissa D, Dvorak Bohuslav

机构信息

Department of Pediatrics, University of Arizona, Tucson, AZ 85724-5073, USA.

出版信息

Semin Perinatol. 2008 Apr;32(2):114-21. doi: 10.1053/j.semperi.2008.01.005.

Abstract

Bile acids (BAs) facilitate emulsification, absorption, and transport of fats and sterols in the intestine and liver and are essential for normal digestion. However, accumulation of BAs in the intestine can result in damage to the intestinal epithelium. Using the neonatal rat model of necrotizing enterocolitis (NEC), we have recently shown that BAs accumulate in both the ileal lumen and enterocytes of neonatal rats with NEC and the increased BA levels are positively correlated with disease severity. Importantly, when BAs are not allowed to accumulate, neonatal rat pups develop significantly less disease. In addition, BA transporters are altered during disease development. These data indicate that BAs play an important role in the development of experimental NEC, and suggest that the inability of neonatal rats to adequately regulate BA transporters may be a mechanism by which ileal damage occurs.

摘要

胆汁酸(BAs)有助于肠道和肝脏中脂肪及固醇的乳化、吸收与转运,对正常消化至关重要。然而,胆汁酸在肠道内蓄积会导致肠上皮受损。利用新生大鼠坏死性小肠结肠炎(NEC)模型,我们最近发现,患有NEC的新生大鼠回肠腔和肠细胞中均有胆汁酸蓄积,且胆汁酸水平升高与疾病严重程度呈正相关。重要的是,若不允许胆汁酸蓄积,新生大鼠幼崽患该病的几率会显著降低。此外,在疾病发展过程中,胆汁酸转运体发生了改变。这些数据表明,胆汁酸在实验性NEC的发展中起重要作用,并提示新生大鼠无法充分调节胆汁酸转运体可能是回肠损伤发生的一种机制。

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本文引用的文献

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