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Arabinoxylan activates lipid catabolism and alleviates liver damage in rats induced by high‐fat diet
Author(s) -
Chen Hong,
Fu Yuanfang,
Jiang Xiujuan,
Li Dongmei,
qin Wen,
Zhang Qing,
Lin Derong,
Liu Yaowen,
Tan Cui,
Huang Zhiqing,
Liu Yuntao,
Chen Daiwen
Publication year - 2018
Publication title -
journal of the science of food and agriculture
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 142
eISSN - 1097-0010
pISSN - 0022-5142
DOI - 10.1002/jsfa.8463
Subject(s) - arabinoxylan , catabolism , triglyceride , lipid peroxidation , medicine , hepatic lipase , endocrinology , chemistry , lipid metabolism , lipoprotein lipase , adipose triglyceride lipase , fatty liver , biochemistry , cholesterol , metabolism , antioxidant , adipose tissue , biology , enzyme , disease
BACKGROUND Arabinoxylan was thought to have the potential to change lipid metabolism and redox homeostasis in human and animal. However, the effect of arabinoxylan on the liver damage induced by high‐fat diet needs further exploiting. RESULTS Six‐weeks‐old 30 male Sprague–Dawley Rats were assigned randomly to three groups ( n = 10 per group), i.e. a control diet (CON) group, a high‐fat diet (HF) group and a high‐fat diet supplemented with arabinoxylan (6% AX, HF‐AX) group. Results showed that final body weight and liver weight were similar in CON group and HF‐AX group, but higher in the HF group. In serum, the HF‐AX group showed lower triglyceride concentrations than did the HF group. In liver, higher lipoprotein lipase, hepatic lipase, total lipase, and acyl‐CoA oxidase activities and lower triglyceride and cholesterol level were observed in the HF‐AX group than in the HF group. For the redox homeostasis, arabinoxylan supplemented in HF increased T‐SOD activity and GSH‐PX activity and reduced MDA + 4‐HNE level in liver and/or compared with those in the HF group. Lipid droplets and liver cell damage were observed in the HF group compared with the CON and HF‐AX groups. CONCLUSION Arabinoxylan could improve lipid metabolic disorder and alleviate liver damage in rats induced by high‐fat diet via activating lipid catabolism and suppressing lipid peroxidation. © 2017 Society of Chemical Industry