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Similar changes in muscle lipid metabolism are induced by chronic high‐fructose feeding and high‐fat feeding in C57 BL /J6 mice
Author(s) -
Song GuangYao,
Ren LuPing,
Chen ShuChun,
Wang Chao,
Liu Na,
Wei LiMin,
Li Fan,
Sun Wen,
Peng LanBo,
Tang Yong
Publication year - 2012
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.12017
Subject(s) - cd36 , medicine , endocrinology , citrate synthase , carnitine , fatty acid synthase , fatty acid , lipid metabolism , biology , peroxisome , fructose , biochemistry , cytochrome c oxidase , chemistry , mitochondrion , enzyme , receptor
Summary The aim of the present study was to investigate the effects of high fructose and high fat feeding on muscle lipid metabolism and to illustrate the mechanisms by which the two different dietary factors induce muscle lipid accumulation. C57 BL /J6 mice were fed either a standard, high‐fructose ( HF ru) or high‐fat diet. After 16 weeks feeding, mice were killed and plasma triglyceride ( TG ) and free fatty acid ( FFA ) levels were detected. In addition, muscle TG and long chain acyl CoA ( LCAC oA) content was determined, glucose tolerance was evaluated and the protein content of fatty acid translocase CD36 (FATCD36) in muscle was measured. Mitochondrial oxidative function in the muscle was evaluated by estimating the activity of oxidative enzymes, namely cytochrome oxidase ( CO x), citrate synthase ( CS ) and β‐hydroxyacyl CoA dehydrogenase (β‐ HAD ), and the muscle protein content of carnitine palmitoyltransferase‐1 ( CPT ‐1), cyclo‐oxygenase ( COX )‐1 and proliferator‐activated receptor coactivator ( PGC )‐1α was determined. Finally, sterol regulatory element‐binding protein‐1c ( SREBP ‐1c ) gene expression and fatty acid synthase ( FAS ) protein content were determined in muscle tissues. After 16 weeks, plasma TG and FFA levels were significantly increased in both the HF ru and HF groups. In addition, mice in both groups exhibited significant increases in muscle TG and LCAC oA content. Compared with mice fed the standard diet (control group), those in the HF ru and HF groups developed glucose intolerance and exhibited increased FATCD 36 protein levels, enzyme activity related to fatty acid utilization in the mitochondria and protein expressions of CPT ‐1, COX ‐1 and PGC ‐1α in muscle tissue. Finally, mice in both the HF ru and HF groups exhibited increase SREBP ‐1c expression and FAS protein content. In conclusion, high fructose and high fat feeding lead to similar changes in muscle lipid metabolism in C57 BL /J6 mice. Lipid accumulation in the muscle may be associated with increased expression of proteins related to lipid transportation and synthesis.