Hepatic PPARγ and LXRα independently regulate lipid accumulation in the livers of genetically obese mice. Issue 14 (21st May 2014)

• Record Type: Journal Article
• Authors: Matsusue, Kimihiko; Aibara, Daisuke; Hayafuchi, Risa; Matsuo, Kohei; Takiguchi, Soichi; Gonzalez, Frank J.; Yamano, Shigeru
• Is Part Of: FEBS letters. Volume 588:Issue 14(2014)
• Page Start: 2277
• Page End: 2281
• Publication Date: 2014-05-21
• Subjects: PPARγ -- peroxisome proliferator-activated receptor γ -- LXRα -- liver X receptor α -- OB/OB -- normal genetic background -- ob/ob -- obese genetic background -- PparγWT -- wild-type PPARγ -- PparγΔH -- hepatocyte-specific PPARγ knockout -- Liver X receptor α -- Peroxisome proliferator-activated receptor γ -- Fatty liver; Biochemistry -- Periodicals; Biophysics -- Periodicals; Molecular biology -- Periodicals; Biochimie -- Périodiques; Biochemistry; Biophysics; Molecular biology; Periodicals; 572.05
• DOI: 10.1016/j.febslet.2014.05.012
• Languages: English
• ISSNs: 0014-5793

Abstract

Abstract : The nuclear hormone receptors liver X receptor α (LXRα) and peroxisome proliferator‐activated receptor γ (PPARγ) play key roles in the development of fatty liver. To determine the link between hepatic PPARγ and LXRα signaling and the development of fatty liver, a LXRα‐specific ligand, T0901317, was administered to normal OB / OB and genetically obese ( ob / ob ) mice lacking hepatic PPARγ ( Pparγ ΔH ). In ob / ob ‐ Pparγ ΔH and OB / OB ‐ Pparγ ΔH mice, as well as ob / ob ‐ Pparγ WT and OB / OB ‐ Pparγ WT mice, the liver weights and hepatic triglyceride levels were markedly increased in response to T0901317 treatment. These results suggest that hepatic PPARγ and LXRα signals independently contribute to the development of fatty liver. Abstract : The role of hepatic PPARγ in LXRα‐associated fat accumulation was determined using mice lacking hepatic PPARγ. The LXR‐specific ligand T0901317 was administered to normal or obesity model mice lacking hepatic PPARγ. The T0901317 increased development of fatty liver in mice lacking hepatic PPARγ. Pathways involving LXRα and PPARγ independently accelerated its development.