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• W4312083503 startingPage "121292" @default.
• W4312083503 abstract "Chronic inflammation plays crucial roles in obesity-induced metabolic diseases. Protein tyrosine phosphatase receptor type O (PTPRO) is a member of the R3 subfamily of receptor-like protein tyrosine phosphatases. We previously suggested a role for PTPRO in the inactivation of the insulin receptor. The present study aimed to elucidate the involvement of PTPRO in the control of glucose and lipid metabolism as well as in obesity-induced systemic inflammation.Lipid accumulation in adipose tissue and the liver, the expression of inflammatory cytokines, and insulin resistance associated with systemic inflammation were investigated in hyper-obese Ptpro-KO mice by feeding a high-fat/high-sucrose diet (HFHSD). The effects of the administration of AKB9778, a specific inhibitor of PTPRO, to ob/ob mice and cultured 3T3-L1 preadipocyte cells were also examined.Ptpro was highly expressed in visceral white adipose tissue and macrophages. Ptpro-KO mice fed HFHSD were hyper-obese, but did not have ectopic fat accumulation in the liver, dysfunctional lipid and glucose homeostasis, systemic inflammation, or insulin resistance. The administration of AKB9778 reproduced the healthy obese phenotypes of Ptpro-KO mice in highly obese ob/ob mice. Furthermore, the inhibition of PTPRO promoted the growth of lipid droplets in adipocytes through an increase in the phosphorylation of Tyr(117) in vimentin.Healthy systemic conditions with the attenuation of inflammation in hyper-obese Ptpro-KO mice were associated with the expansion of adipose tissue and low activation of NF-κb. Therefore, PTPRO may be a promising target to ameliorate hepatic steatosis and metabolic dysfunction." @default.
• W4312083503 created "2023-01-04" @default.
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• W4312083503 date "2023-01-01" @default.
• W4312083503 modified "2023-09-25" @default.
• W4312083503 title "Deletion or inhibition of PTPRO prevents ectopic fat accumulation and induces healthy obesity with markedly reduced systemic inflammation" @default.
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• W4312083503 doi "https://doi.org/10.1016/j.lfs.2022.121292" @default.
• W4312083503 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/36535401" @default.
• W4312083503 hasPublicationYear "2023" @default.
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