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.
Highlights
Short bowel syndrome (SBS) is defined as a malabsorptive state that results from a decreased gut absorptive area following a massive small bowel resection [1,2,3]
parenteral nutrition (PN) can improve the survival of SBS patients, the intestinal adaptation of the remaining bowel segment is still the primary determinant of decreasing malabsorption and malnutrition caused by SBS [5]
The final weight of the rats in the SBS-bile salt dependent lipase (BSDL) group was 25% higher than that in the SBS group (SBS: 134.50 +− 8.38 compared with SBS-BSDL: 168.23 +− 14.42 g, P
Summary
Short bowel syndrome (SBS) is defined as a malabsorptive state that results from a decreased gut absorptive area following a massive small bowel resection (mSBR) [1,2,3]. SBS leads to insufficient nutrient absorption and significant weight loss, and patients must depend on parenteral nutrition (PN) to meet nutritional requirements [4]. PN can improve the survival of SBS patients, the intestinal adaptation of the remaining bowel segment is still the primary determinant of decreasing malabsorption and malnutrition caused by SBS [5]. Several bioactive agents might help to accelerate this adaptive process [6,7,8]. Interventions directed toward improving intestinal adaptation in SBS patients are of immense therapeutic interest
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