Journal
JOURNAL OF GASTROINTESTINAL SURGERY
Volume 18, Issue 2, Pages 286-294Publisher
SPRINGER
DOI: 10.1007/s11605-013-2338-7
Keywords
Short gut syndrome; Small bowel adaptation; High-fat diet; CD36
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Funding
- National Institutes of Health-Morphology and Murine Models Cores of the Digestive Diseases Research Core Center of the Washington University School of Medicine [R01 DK 059288, T32 GM008795, P30DK52574]
- Children's Surgical Sciences Institute of the St. Louis Children's Hospital Foundation
- Marion and Van Black Endowed Pediatric Surgical Fellowship
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Previous studies have shown that high-fat diet (HFD) enhances adaptation if provided immediately following small bowel resection (SBR). The purpose of this study was to determine if HFD could further enhance villus growth after resection-induced adaptation had already taken place. C57/Bl6 mice underwent a 50 % proximal SBR or sham operation and were then provided a standard rodent liquid diet (LD) ad lib. After a typical period of adaptation (7 days), SBR and sham-operated mice were randomized to receive either LD or HFD (42 % kcal fat) for an additional 7 days. Mice were then harvested, and small intestine was collected for analysis. Adaptation occurred in both SBR groups; however, the SBR/HFD had significantly increased villus height compared to SBR/LD. Reverse transcription-polymerase chain reaction of villus enterocytes showed a marked increase in CD36 expression in the SBR/HFD group compared with SBR/LD mice. While exposure to increased enteral fat alone did not affect villus morphology in sham-operated mice, HFD significantly increased villus growth in the setting of resection-induced adaptation, supporting the clinical utility of enteral fat in augmenting adaptation. Increased expression of CD36 suggests a possible mechanistic role in dietary fat metabolism and villus growth in the setting of short gut syndrome.
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