| http://purl.uniprot.org/citations/25843798 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/25843798 | http://www.w3.org/2000/01/rdf-schema#comment | "Hepatic insulin resistance (HIR) is a metabolic abnormality characterized by increased gluconeogenesis which usually contributes from an elevation of free fatty acids. Cannabinoid receptor type 1 (CB1R) and major urinary protein 1 (MUP1) are thought to play pivotal roles in mitochondrial dysfunction, liver steatosis and insulin resistance. The aim of this study was to explore the role of MUP1 in CB1R-mediated HIR through the dysregulation of mitochondrial function in AML12 mouse hepatocytes challenged with high concentration of free fatty acids (HFFA). Firstly we observed that treatment of AM251, a selective CB1R antagonist, obviously reversed the HFFA-induced reduction of MUP1 protein expression both in vivo and in vitro. Additionally, our results revealed that AM251 also reverted HFFA-mediated decrease of the mRNA level of mitochondrial biogenesis-related factors, mtDNA amount, ATP production, mitochondrial respiratory complexes-I and -III, and mitochondrial membrane potential, thus consequently might correlate with a parallel reduction of ROS production. Meanwhile, AM251 attenuated HFFA-induced impairment of insulin signaling phosphorylation and elevation of phosphoenolpyrvate carboxykinase (PEPCK) and glucose 6-phosphatase (G6Pase), two key enzymes of gluconeogenesis. Silence of MUP1 gene abolished the inhibitory effect of AM251 on HFFA-mediated elevation of PEPCK and G6Pase expression, whereas the suppression of insulin signaling and mRNA level of mitochondrial biogenesis-related factors were only partially recovered. Altogether, these findings suggest that the anti-HIR effect of AM251 via improvement of mitochondrial functions might occur in a MUP1-dependent manner."xsd:string |
| http://purl.uniprot.org/citations/25843798 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.bbrc.2015.03.155"xsd:string |
| http://purl.uniprot.org/citations/25843798 | http://purl.uniprot.org/core/author | "Chen C.C."xsd:string |
| http://purl.uniprot.org/citations/25843798 | http://purl.uniprot.org/core/author | "Lin Y.J."xsd:string |
| http://purl.uniprot.org/citations/25843798 | http://purl.uniprot.org/core/author | "Lee T.Y."xsd:string |
| http://purl.uniprot.org/citations/25843798 | http://purl.uniprot.org/core/author | "Ho L.T."xsd:string |
| http://purl.uniprot.org/citations/25843798 | http://purl.uniprot.org/core/author | "Shih K.C."xsd:string |
| http://purl.uniprot.org/citations/25843798 | http://purl.uniprot.org/core/author | "Hsu Y.P."xsd:string |
| http://purl.uniprot.org/citations/25843798 | http://purl.uniprot.org/core/author | "Kwok C.F."xsd:string |
| http://purl.uniprot.org/citations/25843798 | http://purl.uniprot.org/core/date | "2015"xsd:gYear |
| http://purl.uniprot.org/citations/25843798 | http://purl.uniprot.org/core/name | "Biochem Biophys Res Commun"xsd:string |
| http://purl.uniprot.org/citations/25843798 | http://purl.uniprot.org/core/pages | "1063-1068"xsd:string |
| http://purl.uniprot.org/citations/25843798 | http://purl.uniprot.org/core/title | "Major urinary protein 1 interacts with cannabinoid receptor type 1 in fatty acid-induced hepatic insulin resistance in a mouse hepatocyte model."xsd:string |
| http://purl.uniprot.org/citations/25843798 | http://purl.uniprot.org/core/volume | "460"xsd:string |
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