Fructose Ingestion Enhances Atherosclerosis and Deposition of Advanced Glycated End-products in Cholesterol-fed Rabbits

DOI Web Site PubMed 被引用文献10件 参考文献52件
  • Tokita Yoshihisa
    Division of Molecular Metabolism and Diabetes, Tohoku University Graduate School of Medicine, Sendai, Japan.
  • Hirayama Yoshitake
    Laboratory of Biodynamic Chemistry, Graduate School of Life Science and Agriculture, Tohoku University, Sendai, Japan.
  • Sekikawa Akihiro
    Division of Molecular Metabolism and Diabetes, Tohoku University Graduate School of Medicine, Sendai, Japan.
  • Kotake Hidetoshi
    Division of Molecular Metabolism and Diabetes, Tohoku University Graduate School of Medicine, Sendai, Japan.
  • Toyota Takayoshi
    Division of Molecular Metabolism and Diabetes, Tohoku University Graduate School of Medicine, Sendai, Japan.
  • Miyazawa Teruo
    Laboratory of Biodynamic Chemistry, Graduate School of Life Science and Agriculture, Tohoku University, Sendai, Japan.
  • Sawai Takashi
    Department of Pathology, School of Medicine, Iwate Medical University, Morioka, Japan.
  • Oikawa Shinichi
    Division of Endocrinology and Metabolism, Department of Medicine, Nippon Medical School, Tokyo, Japan.

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This study was performed to investigate whether the plasma concentration of phosphatidylcholine hydroperoxide (PCOOH), which is a marker of oxidized stress in the blood, increased in cholesterol-fed rabbits, and fructose ingestion promoted this process and aggravated atherosclerosis. Male Japanese white rabbits (age: 12 weeks, and body weight: around 2.0 kg, n = 15) were divided into three groups, (1) a NN group as a normal control fed a standard diet (n = 5), (2) a CN group fed 1.0% cholesterol, and (3) a CF group given both 1.0% cholesterol and 10% fructose-containing tap water. During 8 weeks, plasma PCOOH levels increased significantly in the CN and CF groups compared to the NN group and fructose further raised the PCOOH level. The atherosclerosis was significantly promoted and the deposition of advanced glycation end products (AGEs) was marked in the CF group compared to the CN group. Fructose worsened the atheromatous lesions caused by cholesterol feeding. The mechanism is most likely through lipid peroxidation, which was increased by cholesterol feeding-induced hyperlipidemia, and the formation of AGEs.

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