DPP4 inhibitor reinforces cell junction proteins in mouse model of short bowel syndrome
link.springer.com shows its articles on its own site.
Read the article on link.springer.com ↗Article · Oct 2019 · 1 min read
In brief
In brief
Study demonstrates that DPP4 inhibitor administration upregulates E-cadherin and occludin expression in a mouse model of short bowel syndrome, potentially strengthening intestinal barrier integrity. By preserving cell junction proteins, DPP4I may reduce bacterial translocation risk in SBS patients through anti-inflammatory mechanisms.
Written by the GCMD Library team from the article.
Abstract
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.