Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10750654 | Biochemical and Biophysical Research Communications | 2015 | 6 Pages |
Abstract
Under normal feeding conditions, oxidative stress stimulates lipid droplets accumulation in hepatocytes. We found that, despite the low visceral fat in Sod1-knockout (KO) mouse, lipid droplets accumulate in the liver to a greater extent than for the wild-type mouse upon fasting. Liver damage became evident in the KO mice. While fasting caused substantial endoplasmic reticulum stress in KO mice, the expression of genes involved in fatty acid production was suppressed. LC3-II, which is essential for the dynamic process of autophagosome formation, was activated in the wild-type mouse and enhanced in the KO mouse. However, the p62, an adapter protein with the ubiquitin- and LC3-binding activity, accumulated abnormally in the livers of KO mice, implying an abortive lipophagic process as the cause for the impaired lipid metabolism and the hepatic damage that occurs upon fasting.
Keywords
apoBTBSALTFASUPRTBSTS1PMTPS2PSCD1stearoyl CoA desaturase 1PBSSREBP1ACCBSAH&EROSAlanine aminotransferasebovine serum albuminApolipoprotein BLiver steatosisfatty acid synthaseTriacylglyceridesTris-buffered salineOxidative stressFastingSite-2 proteaseSite-1 proteaseSODSuperoxide dismutaseendoplasmic reticulumLipophagyPhosphate-buffered salinewild typeHematoxylin and EosinUnfolded protein responsesterol regulatory element binding proteinmicrosomal transfer proteinGluGlucoseReactive oxygen species
Related Topics
Life Sciences
Biochemistry, Genetics and Molecular Biology
Biochemistry
Authors
Toshihiro Kurahashi, Shinji Hamashima, Takaya Shirato, Jaeyong Lee, Takujiro Homma, Eun Sil Kang, Junichi Fujii,