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. C57BL/J6 mice were fed either a standard, high‐fructose (HFru) 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 (LCACoA) 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 (COx), 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 HFru and HF groups. In addition, mice in both groups exhibited significant increases in muscle TG and LCACoA content. Compared with mice fed the standard diet (control group), those in the
HFru and HF groups developed glucose intolerance and exhibited increased FATCD36 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 HFru
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 C57BL/J6 mice. Lipid accumulation in the muscle may be associated
with increased expression of proteins related to lipid transportation and synthesis.
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Document Type: Research Article
Publication date: December 1, 2012