Removal of Visceral Fat Prevents Insulin Resistance and Glucose Intolerance of Aging

  • Ilan Gabriely
    Diabetes Research and Training Center and Division of Endocrinology, Department of Medicine, Albert Einstein College of Medicine, Bronx, New York
  • Xiao Hui Ma
    Diabetes Research and Training Center and Division of Endocrinology, Department of Medicine, Albert Einstein College of Medicine, Bronx, New York
  • Xiao Man Yang
    Diabetes Research and Training Center and Division of Endocrinology, Department of Medicine, Albert Einstein College of Medicine, Bronx, New York
  • Gil Atzmon
    Diabetes Research and Training Center and Division of Endocrinology, Department of Medicine, Albert Einstein College of Medicine, Bronx, New York
  • Michael W. Rajala
    Department of Molecular Pharmacology, Albert Einstein College of Medicine, Bronx, New York
  • Anders H. Berg
    Department of Molecular Pharmacology, Albert Einstein College of Medicine, Bronx, New York
  • Phillip Scherer
    Department of Molecular Pharmacology, Albert Einstein College of Medicine, Bronx, New York
  • Luciano Rossetti
    Diabetes Research and Training Center and Division of Endocrinology, Department of Medicine, Albert Einstein College of Medicine, Bronx, New York
  • Nir Barzilai
    Diabetes Research and Training Center and Division of Endocrinology, Department of Medicine, Albert Einstein College of Medicine, Bronx, New York

抄録

<jats:p>Age-dependent changes in insulin action and body fat distribution are risk factors for the development of type 2 diabetes. To examine whether the accumulation of visceral fat (VF) could play a direct role in the pathophysiology of insulin resistance and type 2 diabetes, we monitored insulin action, glucose tolerance, and the expression of adipo-derived peptides after surgical removal of VF in aging (20-month-old) F344/Brown Norway (FBN) and in Zucker Diabetic Fatty (ZDF) rats. As expected, peripheral and hepatic insulin action were markedly impaired in aging FBN rats, and extraction of VF (accounting for ∼18% of their total body fat) was sufficient to restore peripheral and hepatic insulin action to the levels of young rats. When examined at the mechanistic level, removal of VF in ZDF rats prevented the progressive decrease in insulin action and delayed the onset of diabetes, but VF extraction did not alter plasma free fatty acid levels. However, the expression of tumor necrosis factor-α and leptin in subcutaneous (SC) adipose tissue were markedly decreased after VF removal (by approximately three- and twofold, respectively). Finally, extracted VF retained ∼15-fold higher resistin mRNA compared with SC fat. Our data suggest that insulin resistance and the development of diabetes can be significantly reduced in aging rats by preventing the age-dependent accumulation of VF. This study documents a cause-and-effect relationship between VF and major components of the metabolic syndrome.</jats:p>

収録刊行物

  • Diabetes

    Diabetes 51 (10), 2951-2958, 2002-10-01

    American Diabetes Association

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