ArticleSurgery2011
Administration of a dipeptidyl peptidase IV inhibitor enhances the intestinal adaptation in a mouse model of short bowel syndrome.
Article in Surgery, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
- Biological Insights into Intestinal Adaptation from Preclinical Models of Short Bowel Syndrome.Cells · 2026Review
- Colonic Adaptation Postileal Resection: Bile Acid Absorption in an Ileal Resection Mouse Model.Gastroenterology research and practice · 2025Article
- Decreased liver damage in rat models of short bowel syndrome through DPP4 inhibition.Pediatric surgery international · 2022Article
- Chronic intestinal failure and short bowel syndrome in Crohn's disease.World journal of gastroenterology · 2021Review
- DPP4 inhibitor reinforces cell junction proteins in mouse model of short bowel syndrome.Pediatric surgery international · 2020Article
- The Long Road to the Development of Effective Therapies for the Short Gut Syndrome: A Personal Perspective.Digestive diseases and sciences · 2019Review
- Differential action of TGR5 agonists on GLP-2 secretion and promotion of intestinal adaptation in a piglet short bowel model.American journal of physiology. Gastrointestinal and liver physiology · 2019Article
- Bile salt dependent lipase promotes intestinal adaptation in rats with massive small bowel resection.Bioscience reports · 2018Article
- Interdependency of EGF and GLP-2 Signaling in Attenuating Mucosal Atrophy in a Mouse Model of Parenteral Nutrition.Cellular and molecular gastroenterology and hepatology · 2017Article
- Gastrointestinal Endogenous Protein-Derived Bioactive Peptides: An in Vitro Study of Their Gut Modulatory Potential.International journal of molecular sciences · 2016Article
- Adult zebrafish intestine resection: a novel model of short bowel syndrome, adaptation, and intestinal stem cell regeneration.American journal of physiology. Gastrointestinal and liver physiology · 2015Article
- Animal models of gastrointestinal and liver diseases. Animal models of infant short bowel syndrome: translational relevance and challenges.American journal of physiology. Gastrointestinal and liver physiology · 2014Review
- Pharmacology, physiology, and mechanisms of action of dipeptidyl peptidase-4 inhibitors.Endocrine reviews · 2014Review
- Dipeptidyl peptidase IV inhibition prevents the formation and promotes the healing of indomethacin-induced intestinal ulcers in rats.Digestive diseases and sciences · 2014Article
- GLP-2 delays but does not prevent the onset of necrotizing enterocolitis in preterm pigs.Journal of pediatric gastroenterology and nutrition · 2013Article
- Dipeptidyl peptidase IV inhibition potentiates amino acid- and bile acid-induced bicarbonate secretion in rat duodenum.American journal of physiology. Gastrointestinal and liver physiology · 2012Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundGlucagon-like peptide-2 induces small intestine mucosal epithelial cell proliferation and may have benefit for patients who suffer from short bowel syndrome. However, glucagon-like peptide-2 is inactivated rapidly in vivo by dipeptidyl peptidase IV. Therefore, we hypothesized that selectively inhibiting dipeptidyl peptidase IV would prolong the circulating life of glucagon-like peptide-2 and lead to increased intestinal adaptation after development of short bowel syndrome.
methodsEight-week old C57BL/6J mice underwent a 50% proximal small bowel resection and were treated with either sitagliptin, a dipeptidyl peptidase IV-inhibitor, starting 1 day before surgery versus placebo. The efficacy of dipeptidyl peptidase IV-inhibitor was assessed 3 days after resection, including intestinal morphology, epithelial cell apoptosis, and epithelial cell proliferation. Adaptive mechanisms were assessed with quantitative real-time polymerase chain reaction, and plasma bioactive glucagon-like peptide-2 was measured by radioimmunoassay.
resultsBody weight loss and peripheral blood glucose levels did not change compared with short bowel syndrome controls. Dipeptidyl peptidase IV-inhibitor treatment led to significant increases in villus height and crypt depth. Dipeptidyl peptidase IV-inhibitor treatment did not change EC apoptosis rates significantly, but it did increase crypt epithelial cell proliferation significantly versus placebo-short bowel syndrome controls. Dipeptidyl peptidase IV-inhibitor treatment markedly increased messenger RNA expression of β-catenin and c-myc in ileal mucosa. Plasma glucagon-like peptide-2 levels increased significantly (∼ 40.9%) in dipeptidyl peptidase IV-inhibitor short bowel syndrome mice.
conclusionDipeptidyl peptidase IV-inhibitor treatment increased short bowel syndrome adaptation and might potentially be useful for short bowel syndrome patients.
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Registered trials
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