Obesity is one of the major epidemics of this millennium, and its incidence is growing worldwide. Following the epidemics of obesity, nonalcoholic fatty liver disease (NAFLD) has become a disease of increasing prevalence and a leading cause of morbidity and mortality closely related to cardiovascular disease, malignancies, and cirrhosis. It is believed that oxidative stress is a main player in the development and progression of NAFLD. Currently, a pharmacological approach has become necessary in NAFLD because of a failure to modify lifestyle and dietary habits in most patients. Vitamin E is a potent antioxidant that has been shown to reduce oxidative stress in NAFLD. This review summarizes the biological activities of vitamin E, with a primary focus on its therapeutic efficacy in NAFLD.
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http://dx.doi.org/10.3390/antiox7010012 | DOI Listing |
Eur J Prev Cardiol
January 2025
Department of Clinical Sciences and Community Health, University of Milan, Via Commenda 19, Milan 20122, Italy.
Liver Int
February 2025
Department of Occupational Health and Environmental Health, School of Public Health, Capital Medical University, Beijing, China.
Background: Metabolic associated fatty liver disease (MAFLD), previously defined as non-alcoholic fatty liver disease (NAFLD), has been shown to be closely related to many environmental pollutants. Lately, we found methyl tert-butyl ether (MTBE), a new environmental pollutant, could increase NAFLD risk in American adults, which still needs more population epidemiological studies to verify, and its pathogenic mechanism is not yet clear.
Methods: We conducted a cross-sectional study among petrol station workers, diagnosed their MAFLD according to internationally recognised diagnostic criteria, assessed the potential association of MTBE exposure with MAFLD risk, and explored the miR-18a-5p/PXR/SREBP2 pathway as possible pathogenic mechanisms in male Wistar rats and HepaRG cells treated with MTBE.
Nutr Rev
January 2025
Faculty of Medicine, Pelita Harapan University, Tangerang, Banten 15811, Indonesia.
The demonization of seed oils "campaign" has become stronger over the decades. Despite the dietary guidelines provided by nutritional experts recommending the limiting of saturated fat intake and its replacement with unsaturated fat-rich food sources, some health experts ignore the dietary guidelines and the available human research evidence, suggesting the opposite. As contrarians, these individuals could easily shift public opinion so that dietary behavior moves away from intake of unsaturated fat-rich food sources (including seed oils) toward saturated fats, which is very concerning.
View Article and Find Full Text PDFNaunyn Schmiedebergs Arch Pharmacol
January 2025
Department of Pharmacology and Toxicology, Faculty of Pharmacy (Boys), Al-Azhar University, Nasr City, 11651, Cairo, Egypt.
The clinical use of dexamethasone (DXM) is associated with the development of non-alcoholic fatty liver disease (NAFLD). However, the mechanisms by which DXM-induced NAFLD is still incompletely known. Therefore, the current study aims to test the hypothesis that DXM-induced NAFLD is mediated by dysregulation of key genes involved in lipid metabolism and liraglutide (LG) can ameliorate these effects.
View Article and Find Full Text PDFNan Fang Yi Ke Da Xue Xue Bao
January 2025
Department of Gastroenterology, Affiliated Hospital of Guizhou Medical University, Guiyang 550000, China.
Objectives: To investigate the regulatory role of nucleotide-bound oligomerized domain-like receptor containing pyrin-domain protein 6 (NLRP6) in liver lipid metabolism and non-alcoholic fatty liver disease (NAFLD).
Methods: Mouse models with high-fat diet (HFD) feeding for 16 weeks (=6) or with methionine choline-deficient diet (MCD) feeding for 8 weeks (=6) were examined for the development of NAFLD using HE and oil red O staining, and hepatic expressions of NLRP6 were detected with RT-qPCR, Western blotting, and immunohistochemical staining. Cultured human hepatocytes (LO2 cells) with adenovirus-mediated NLRP6 overexpression or knock-down were treated with palmitic acid (PA) in the presence or absence of compound C (an AMPK inhibitor), and the changes in cellular lipid metabolism were examined by measuring triglyceride, ATP and β-hydroxybutyrate levels and using oil red staining, RT-qPCR, and Western blotting.
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