期刊
JOURNAL OF NUTRITIONAL BIOCHEMISTRY
卷 38, 期 -, 页码 70-80出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.jnutbio.2016.08.013
关键词
Walnut; High-fat diet; Liver; CYP2E1; Oxidative stress; JNK; Apoptosis
资金
- Intramural Research Program of the National Institute on Alcohol Abuse and Alcoholism
- KRIBB Research Initiative Program (Korean Biomedical Scientist Fellowship Program)
- Korea Research Institute of Bioscience and Biotechnology, Republic of Korea
We hypothesized that dietary walnut would prevent high-fat-diet (HFD)-induced hepatic apoptosis based on its antioxidant properties. Male C57BL/6J mice were fed a rodent chow or HFD (45% energy-derived)+/- walnuts (21.5% energy-derived) for 6 weeks. Liver histological and biochemical analyses revealed significantly elevated fat accumulation in mice fed HFD compared to mice fed the chow or HFD +/- walnuts. Walnut supplementation prevented HFD-mediated alteration of the levels of key proteins in lipid homeostasis such as Sirt1, AMPK and FAS, leading to decreased fat accumulation. In addition, walnut supplementation to HFD significantly decreased the hepatic levels of cytochrome P450-2E1, nitrated proteins and lipid peroxidation. Furthermore, walnut supplementation decreased the activated cell-death-associated p-JNK and p-p38K accompanied with increased hepatocyte apoptosis in HFD group. The beneficial effects of dietary walnut likely result, at least partially, from its antioxidant ingredients and attenuating HFD-induced hepatic steatosis, nitroxidative stress and apoptosis. Published by Elsevier Inc.
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