Ameliorative Effects of Mulberry (Morus alba L.) Leaves on Hyperlipidemia in Rats Fed a High-Fat Diet: Induction of Fatty Acid Oxidation, Inhibition of Lipogenesis, and Suppression of Oxidative Stress

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  • KOBAYASHI Yukihiro
    Chemistry Division, Kanagawa Prefectural Institute of Public Health
  • MIYAZAWA Maki
    Chemistry Division, Kanagawa Prefectural Institute of Public Health
  • KAMEI Asuka
    Food Safety and Reliability Project, Kanagawa Academy of Science and Technology
  • ABE Keiko
    Food Safety and Reliability Project, Kanagawa Academy of Science and Technology Department of Applied Biological Chemistry, Graduate School of Agricultural and Life Sciences, The University of Tokyo
  • KOJIMA Takashi
    Chemistry Division, Kanagawa Prefectural Institute of Public Health

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  • Ameliorative Effects of Mulberry (<i>Morus alba</i>L.) Leaves on Hyperlipidemia in Rats Fed a High-Fat Diet: Induction of Fatty Acid Oxidation, Inhibition of Lipogenesis, and Suppression of Oxidative Stress

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To determine the effects of mulberry (Morus alba L.) leaves on hyperlipidemia, we performed gene expression profiling of the liver. Rats were fed a high-fat diet and administered mulberry leaves for 7 weeks. Plasma triglyceride and non-esterified fatty acid levels were significantly lower in the rats treated with mulberry leaves as compared with the untreated rats. DNA microarray analysis revealed that mulberry leaves upregulated expression of the genes involved in α-, β- and ω-oxidation of fatty acids, mainly related to the peroxisome proliferator-activated receptor signaling pathway, and downregulated the genes involved in lipogenesis. Furthermore, treatment with mulberry leaves upregulated expression of the genes involved in the response to oxidative stress. These results indicate that consumption of fatty acids and inhibition of lipogenesis are responsible for the reduction in plasma lipids caused by mulberry administration. In addition, mulberry treatment maintains the body’s oxidative state at a low level despite enhancing fatty acid oxidation.

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