{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Chang YC"],"funding":["National Taiwan University Hospital","NIDDK NIH HHS","National Taiwan University Hospital (NTUH)","National Science and Technology Council","National Science and Technology Council (NSTC)"],"pagination":["938-966"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12081876"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["17(5)"],"pubmed_abstract":["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 d"],"journal":["EMBO molecular medicine"],"pubmed_title":["Identification of PTGR2 inhibitors as a new therapeutic strategy for diabetes and obesity."],"pmcid":["PMC12081876"],"funding_grant_id":["R01 DK132469","R01 DK133528","UN105-0072,UN109-008","104-2314-B-002-219-MY3,106-2314-B-002-137-MY3,106-2321-B-002-040,107-2321-B-002-067"],"pubmed_authors":["Chen YA","Li FA","Chiu CH","Hung MS","Yeh TK","Hee SW","Hsu CN","Cheng TR","Chuang LM","Ke YY","Shih SF","Chen TY","Yen HY","Hu CM","Huang JY","Chang CF","Lee HL","Vogel U","Tseng YH","Lin SW","Liao KC","Lin SY","Tsou LK","Chen SY","Saar D","Laio D","Hwang JJ","Chang YC","Chen YR","Hsieh ML","Kragelund BB","Chou YW","Hung AF"],"additional_accession":[]},"is_claimable":false,"name":"Identification of PTGR2 inhibitors as a new therapeutic strategy for diabetes and obesity.","description":"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 d","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 May","modification":"2026-04-08T19:51:23.506Z","creation":"2026-04-08T14:31:15.146Z"},"accession":"S-EPMC12081876","cross_references":{"pubmed":["40119175"],"doi":["10.1038/s44321-025-00216-4"]}}