Bile salt dependent lipase promotes intestinal adaptation in rats with massive small bowel resection

Biosci Rep. 2018 May 31;38(3):BSR20180077. doi: 10.1042/BSR20180077. Print 2018 Jun 29.

Abstract

Intestinal adaptation is important for the short bowel syndrome (SBS) patients. Growing evidence has suggested that bile salt dependent lipase (BSDL) not only has the lipolytic activity, but also the immune-modulating and pro-proliferative activities. The purpose of the present study was to investigate the effects of BSDL on intestinal adaptive growth and gut barrier function in a rat model of SBS. Twenty-four male Sprague-Dawley rats were randomly divided into three experimental groups: sham group (rats underwent bowel transection and re-anastomosis), SBS group (rats underwent 80% bowel resection), SBS-BSDL group (SBS rats orally administered BSDL). The animals were weighed daily. The intestinal morpho-histochemical changes and intestinal barrier function were determined 14 days after the operations. Meanwhile, the expressions of Wnt signaling molecules in enterocytes were also analyzed by immunohistochemistry and Western blot. The postoperative weight gain was faster in the SBS rats treated with BSDL than in the SBS/untreated group. The SBS rats treated with BSDL had significantly greater villus height, crypt depth, and enterocyte proliferation in their residual intestines, as compared with the SBS/untreated group. The recovery of intestinal barrier function was promoted and the expressions of tight-junction proteins were increased in the SBS rats treated with BSDL. Additionally, the data indicated that the proadaptive activities of BSDL might be mediated by Wnt signaling activation in the enterocytes. These observations suggested that enteral BSDL administration promoted intestinal adaptive growth and barrier repairing by activating Wnt signaling pathway in SBS rats.

Keywords: Wnt/beta-catenin signaling; bile salt dependent lipase; intestinal adaptation; intestinal barrier; short bowel syndrome.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / genetics
  • Bile Acids and Salts
  • Cell Proliferation / genetics
  • Disease Models, Animal
  • Humans
  • Immunomodulation / genetics
  • Intestinal Mucosa / enzymology*
  • Intestinal Mucosa / growth & development
  • Intestinal Mucosa / immunology
  • Intestinal Mucosa / surgery
  • Intestine, Small / growth & development
  • Intestine, Small / surgery*
  • Intestines
  • Rats
  • Rats, Sprague-Dawley
  • Short Bowel Syndrome / enzymology*
  • Short Bowel Syndrome / immunology
  • Short Bowel Syndrome / pathology
  • Sterol Esterase / genetics*
  • Sterol Esterase / immunology

Substances

  • Bile Acids and Salts
  • bile salt-stimulated lipase
  • Sterol Esterase