スエヨシ　リヨウ   末吉　亮    所属   医学部 医学科（東京女子医科大学病院）    職種   講師
論文種別	原著
言語種別	英語
査読の有無	査読あり
表題	DPP4 inhibitor reinforces cell junction proteins in mouse model of short bowel syndrome.
掲載誌名	正式名：Pediatric surgery international 略　 称：Pediatr Surg Int ISSNコード：14379813/01790358
掲載区分	国外
巻・号・頁	36(1),pp.49-55
著者・共著者	Sueyoshi Ryo†, Miyahara Katsumi, Nakazawa-Tanaka Nana, Fujiwara Naho, Ochi Takanori, Yamataka Atsuyuki
担当区分	筆頭著者
発行年月	2020/01
概要	PURPOSE:Bacterial overgrowth commonly occurs and favors bacterial translocation in short bowel syndrome (SBS). Glucagon-like peptide-2 (GLP-2) is effective for treating SBS, but is rapidly inactivated by dipeptidyl peptidase IV (DPP4). DPP4 inhibitor (DPP4I) is known to be effective for treating SBS. Here, we investigated cell junction protein function following DPP4I administration in a mouse model of SBS.METHODS:Mice were divided into four groups: naïve (n = 5), naïve + DPP4I (n = 6), control (n = 6), and DPP4I (n = 5). All control and DPP4I mice had 50% of their proximal small bowel resected. DPP4I or normal saline was administered orally twice daily from days 1-7 postoperatively. The functions of cell junction proteins were assessed by RT-PCR and immunohistochemistry. Body weights and blood glucose levels were recorded.RESULTS:E-Cadherin was significantly higher in the DPP4I group than in the control group. E-Cadherin, occludin, and claudin-4 were significantly higher in the naïve group than in the control group. Positive staining for E-cadherin and occludin varied widely between the control and DPP4I groups.CONCLUSION:Up-regulation of E-cadherin and occludin by DPP4I may be correlated with the anti-inflammatory action of DPP4I. Therefore, DPP4I may reduce bacterial translocation in SBS.
DOI	10.1007/s00383-019-04571-5
PMID	31576468