Next Article in Journal
Structure of Staphylococcal Enterotoxin N: Implications for Binding Properties to Its Cellular Proteins
Next Article in Special Issue
Anti-Inflammatory and Antioxidant Properties of Dehydrated Potato-Derived Bioactive Compounds in Intestinal Cells
Previous Article in Journal
McArdle Disease: New Insights into Its Underlying Molecular Mechanisms
Previous Article in Special Issue
Adipose Tissue Mitochondrial Factors Profile after Dietary Bioactive Compound Weight Reduction Treatments in a Mice Obesity Model
Open AccessReview

Impact of Glucoraphanin-Mediated Activation of Nrf2 on Non-Alcoholic Fatty Liver Disease with a Focus on Mitochondrial Dysfunction

by 1,2, 2 and 2,3,*
1
Key Laboratory of Laboratory Medicine, School of Laboratory Medicine and Life Science, Wenzhou Medical University, Wenzhou 325035, China
2
Department of Cell Metabolism and Nutrition, Advanced Preventive Medical Sciences Research Center, Kanazawa University, Kanazawa, Ishikawa 920-8640, Japan
3
Division of Metabolism and Biosystemic Science, Department of Medicine, Asahikawa Medical University, Asahikawa, Hokkaido 078-8510, Japan
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2019, 20(23), 5920; https://doi.org/10.3390/ijms20235920
Received: 31 October 2019 / Revised: 19 November 2019 / Accepted: 23 November 2019 / Published: 25 November 2019
(This article belongs to the Special Issue Targeted Protection of Bioactive Compounds to Mitochondria)
Non-alcoholic fatty liver disease (NAFLD) is a common disease in Western nations and ranges in severity from steatosis to steatohepatitis (NASH). NAFLD is a genetic-environmental-metabolic stress-related disease of unclear pathogenesis. NAFLD is triggered by caloric overconsumption and physical inactivity, which lead to insulin resistance and oxidative stress. A growing body of evidence indicates that mitochondrial dysfunction plays a critical role in the pathogenesis of NAFLD. Mitochondrial dysfunction not only promotes fat accumulation, but also leads to generation of reactive oxygen species (ROS) and lipid peroxidation, resulting in oxidative stress in hepatocytes. Nuclear factor erythroid 2-related factor 2 (Nrf2) is an important modulator of antioxidant signaling that serves as a primary cellular defense against the cytotoxic effects of oxidative stress. The pharmacological induction of Nrf2 ameliorates obesity-associated insulin resistance and NAFLD in a mouse model. Sulforaphane and its precursor glucoraphanin are derived from broccoli sprouts and are the most potent natural Nrf2 inducers—they may protect mitochondrial function, thus suppressing the development of NASH. In this review, we briefly describe the role of mitochondrial dysfunction in the pathogenesis of NASH and the effects of glucoraphanin on its development. View Full-Text
Keywords: nonalcoholic fatty liver disease (NAFLD); insulin resistance; chronic inflammation; mitochondrial dysfunction; Nrf2; sulforaphane; glucoraphanin nonalcoholic fatty liver disease (NAFLD); insulin resistance; chronic inflammation; mitochondrial dysfunction; Nrf2; sulforaphane; glucoraphanin
Show Figures

Figure 1

MDPI and ACS Style

Xu, L.; Nagata, N.; Ota, T. Impact of Glucoraphanin-Mediated Activation of Nrf2 on Non-Alcoholic Fatty Liver Disease with a Focus on Mitochondrial Dysfunction. Int. J. Mol. Sci. 2019, 20, 5920.

Show more citation formats Show less citations formats
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
Search more from Scilit
 
Search
Back to TopTop