Next Article in Journal
Serum Albumin Redox States: More Than Oxidative Stress Biomarker
Next Article in Special Issue
Molecular Insight into the Regulation of Vimentin by Cysteine Modifications and Zinc Binding
Previous Article in Journal
Characterization of NADPH Oxidase Expression and Activity in Acute Myeloid Leukemia Cell Lines: A Correlation with the Differentiation Status
Previous Article in Special Issue
CFTR Modulator Therapy with Lumacaftor/Ivacaftor Alters Plasma Concentrations of Lipid-Soluble Vitamins A and E in Patients with Cystic Fibrosis
Article

Reduced Liver Autophagy in High-Fat Diet Induced Liver Steatosis in New Zealand Obese Mice

by 1,2, 1,2, 1,3, 1,2,3,4,5,* and 1,3
1
Department of Molecular Toxicology, German Institute of Human Nutrition, Potsdam-Rehbruecke, 14558 Nuthetal, Germany
2
German Center for Diabetes Research (DZD), 85764 München-Neuherberg, Germany
3
German Center for Cardiovascular Research (DZHK—Partner Site Berlin), 10117 Berlin, Germany
4
Department of Physiological Chemistry, Faculty of Chemistry, University of Vienna, 1090 Vienna, Austria
5
Institute of Nutritional Sciences, University of Potsdam, 14558 Nuthetal, Germany
*
Author to whom correspondence should be addressed.
Academic Editors: Han Moshage, Bresgen Nikolaus and Werner Siems
Antioxidants 2021, 10(4), 501; https://doi.org/10.3390/antiox10040501
Received: 15 February 2021 / Revised: 4 March 2021 / Accepted: 17 March 2021 / Published: 24 March 2021
(This article belongs to the Special Issue Commemorative Issue of Antioxidants Dedicated to Peter Eckl)
Non-alcoholic fatty liver disease (NAFLD), as a consequence of overnutrition caused by high-calorie diets, results in obesity and disturbed lipid homeostasis leading to hepatic lipid droplet formation. Lipid droplets can impair hepatocellular function; therefore, it is of utmost importance to degrade these cellular structures. This requires the normal function of the autophagic-lysosomal system and the ubiquitin-proteasomal system. We demonstrated in NZO mice, a polygenic model of obesity, which were compared to C57BL/6J (B6) mice, that a high-fat diet leads to obesity and accumulation of lipid droplets in the liver. This was accompanied by a loss of autophagy efficiency whereas the activity of lysosomal proteases and the 20S proteasome remained unaffected. The disturbance of cellular protein homeostasis was further demonstrated by the accumulation of 3-nitrotyrosine and 4-hydroxynonenal modified proteins, which are normally prone to degradation. Therefore, we conclude that fat accumulation in the liver due to a high-fat diet is associated with a failure of autophagy and leads to the disturbance of proteostasis. This might further contribute to lipid droplet stabilization and accumulation. View Full-Text
Keywords: proteostasis; protein modification; 4-HNE; proteasome; lipid droplets proteostasis; protein modification; 4-HNE; proteasome; lipid droplets
Show Figures

Figure 1

MDPI and ACS Style

Korovila, I.; Höhn, A.; Jung, T.; Grune, T.; Ott, C. Reduced Liver Autophagy in High-Fat Diet Induced Liver Steatosis in New Zealand Obese Mice. Antioxidants 2021, 10, 501. https://doi.org/10.3390/antiox10040501

AMA Style

Korovila I, Höhn A, Jung T, Grune T, Ott C. Reduced Liver Autophagy in High-Fat Diet Induced Liver Steatosis in New Zealand Obese Mice. Antioxidants. 2021; 10(4):501. https://doi.org/10.3390/antiox10040501

Chicago/Turabian Style

Korovila, Ioanna, Annika Höhn, Tobias Jung, Tilman Grune, and Christiane Ott. 2021. "Reduced Liver Autophagy in High-Fat Diet Induced Liver Steatosis in New Zealand Obese Mice" Antioxidants 10, no. 4: 501. https://doi.org/10.3390/antiox10040501

Find Other Styles
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Back to TopTop