Preventive effects of dietary walnuts on high-fat-induced hepatic fat accumulation, oxidative stress and apoptosis in mice

被引:27
|
作者
Choi, Youngshim [1 ]
Abdelmegeed, Mohamed A. [1 ]
Song, Byoung-Joon [1 ]
机构
[1] NIAAA, Sect Mol Pharmacol & Toxicol, Lab Membrane Biochem & Biophys, 9000 Rockville Pike, Bethesda, MD 20892 USA
来源
关键词
Walnut; High-fat diet; Liver; CYP2E1; Oxidative stress; JNK; Apoptosis; NITRIC-OXIDE SYNTHASE; MITOCHONDRIAL RESPIRATORY-CHAIN; LIVER-DISEASE; HEPATOCYTE APOPTOSIS; CYTOCHROME-P450; 2E1; LIPID-PEROXIDATION; NONALCOHOLIC STEATOHEPATITIS; ENDOTHELIAL FUNCTION; INSULIN-RESISTANCE; ACID-METABOLISM;
D O I
10.1016/j.jnutbio.2016.08.013
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:70 / 80
页数:11
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