國家衛生研究院 NHRI:Item 3990099045/17014
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    題名: Identification of PTGR2 inhibitors as a new therapeutic strategy for diabetes and obesity
    作者: Chang, YC;Hsieh, ML;Lee, HL;Hee, SW;Chang, CF;Yen, HY;Chen, YA;Chen, YR;Chou, YW;Li, FA;Ke, YY;Chen, SY;Hung, MS;Hung, AF;Huang, JY;Chiu, CH;Lin, SY;Shih, SF;Hsu, CN;Hwang, JJ;Yeh, TK;Cheng, TR;Liao, KC;Laio, D;Lin, SW;Chen, TY;Hu, CM;Vogel, U;Saar, D;Kragelund, BB;Tsou, LK;Tseng, YH;Chuang, LM
    貢獻者: Institute of Biotechnology and Pharmaceutical Research
    摘要: Peroxisome proliferator-activated receptor γ (PPARγ) is a master transcriptional regulator of systemic insulin sensitivity and energy balance. The anti-diabetic drug thiazolidinediones (TZDs) are potent synthetic PPARγ ligands with undesirable side effects, including obesity, fluid retention, and osteoporosis. 15-keto prostaglandin E2 (15-keto-PGE2) is an endogenous PPARγ ligand metabolized by prostaglandin reductase 2 (PTGR2). Here, we confirmed that 15-keto-PGE2 binds to and activates PPARγ via covalent binding. In patients with type 2 diabetes and obese mice, serum 15-keto-PGE2 levels were decreased. Administration of 15-keto-PGE2 improves glucose homeostasis and prevented diet-induced obesity in mice. Either genetic inhibition of PTGR2 or PTGR2 inhibitor BPRPT0245 protected mice from diet-induced obesity, insulin resistance, and hepatic steatosis without causing fluid retention and osteoporosis. In conclusion, inhibition of PTGR2 is a new therapeutic approach to treat diabetes and obesity through increasing endogenous PPARγ ligands while avoiding side effects including increased adiposity, fluid retention, and osteoporosis.
    日期: 2025-03-21
    關聯: EMBO Molecular Medicine. 2025 Mar 21;Article in Press.
    Link to: http://dx.doi.org/10.1038/s44321-025-00216-4
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=1757-4676&DestApp=IC2JCR
    Cited Times(Scopus): https://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=105000556051
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