Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz
Gewählte Publikation:
SHR Neuro Krebs Kardio Lipid Stoffw Microb
Chow, JD; Lawrence, RT; Healy, ME; Dominy, JE; Liao, JA; Breen, DS; Byrne, FL; Kenwood, BM; Lackner, C; Okutsu, S; Mas, VR; Caldwell, SH; Tomsig, JL; Cooney, GJ; Puigserver, PB; Turner, N; James, DE; Villén, J; Hoehn, KL.
Genetic inhibition of hepatic acetyl-CoA carboxylase activity increases liver fat and alters global protein acetylation.
Mol Metab. 2014; 3(4):419-431
Doi: 10.1016/j.molmet.2014.02.004
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- Lackner Karoline
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- Abstract:
- Lipid deposition in the liver is associated with metabolic disorders including fatty liver disease, type II diabetes, and hepatocellular cancer. The enzymes acetyl-CoA carboxylase 1 (ACC1) and ACC2 are powerful regulators of hepatic fat storage; therefore, their inhibition is expected to prevent the development of fatty liver. In this study we generated liver-specific ACC1 and ACC2 double knockout (LDKO) mice to determine how the loss of ACC activity affects liver fat metabolism and whole-body physiology. Characterization of LDKO mice revealed unexpected phenotypes of increased hepatic triglyceride and decreased fat oxidation. We also observed that chronic ACC inhibition led to hyper-acetylation of proteins in the extra-mitochondrial space. In sum, these data reveal the existence of a compensatory pathway that protects hepatic fat stores when ACC enzymes are inhibited. Furthermore, we identified an important role for ACC enzymes in the regulation of protein acetylation in the extra-mitochondrial space.
- Find related publications in this database (Keywords)
- Lipid metabolism
- Liver
- Steatosis: Acetylation