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• W3045944878 abstract "Abstract Aims To investigate the effect of anagliptin (Ana), a dipeptidyl peptidase‐4 (DPP‐4) inhibitor, on acute ischemia‐induced bladder dysfunction in rats. Methods Eight‐week‐old female Wistar‐ST rats were randomly assigned into four groups: (a) sham; (b) ligation (Lig); (c) Lig + Ana; and (d) Lig + Liraglutide (a glucagon‐like peptide‐1 [GLP‐1] receptor agonist; Lira). Rats in the Lig, Lig + Ana, and Lig + Lira groups underwent ligature of the bilateral internal iliac arteries. Ana was orally administered mixed with the CE‐2 diet. Lira was subcutaneously administered once a day. Blood glucose levels, plasma dipeptidyl peptidase 4 (DPP‐4) activity, GLP‐1 levels, and bladder function were measured in all groups. Bladder blood flow was measured in the sham, Lig, and Lig + Ana groups, 4 weeks postsurgery. Results No differences in blood glucose levels among the groups were observed. DPP‐4 activity decreased in the Lig + Ana group ( P < .01). GLP‐1 levels in the Lig + Ana and Lig + Lira groups were higher than those in the sham and Lig groups ( P < .01). Intercontraction intervals (ICIs) were longer in the Lig and Lig + Lira groups than in the sham group ( P < .05), but similar to those observed in the Lig + Ana and sham groups. The Lig group exhibited reduced bladder blood flow relative to the sham group ( P < .01); however, this measure improved in the Lig + Ana group ( P < .01). Conclusions Ana administration improved ICIs and bladder blood flow after acute bladder ischemia through a GLP‐1 receptor‐independent signaling pathway, without altering the blood glucose levels. Therefore, Ana dosing might be useful to prevent ischemia‐induced bladder dysfunctions." @default.
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• W3045944878 date "2020-07-29" @default.
• W3045944878 modified "2023-09-25" @default.
• W3045944878 title "Anagliptin, a dipeptidyl peptidase‐4 inhibitor, improved bladder function and hemodynamics in rats with bilateral internal iliac artery ligation" @default.
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• W3045944878 doi "https://doi.org/10.1002/nau.24449" @default.
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