Fenofibrate increases serum vaspin by upregulating its expression in adipose tissue

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• 作者：Mingwei Chen (1) (2) (4)
  Datong Deng (1) (2)
  Zhaohui Fang (3)
  Ming Xu (1) (2)
  Honglin Hu (1) (2)
  Li Luo (1) (2)
  Youmin Wang (1) (2) (4)
  
• 关键词：Vaspin ; Adipokines ; Insulin resistance ; Visceral obesity
• 刊名：Endocrine
• 出版年：2014
• 出版时间：April 2014
• 年：2014
• 卷：45
• 期：3
• 页码：409-421
• 全文大小：640 KB
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• 作者单位：Mingwei Chen (1) (2) (4)
  Datong Deng (1) (2)
  Zhaohui Fang (3)
  Ming Xu (1) (2)
  Honglin Hu (1) (2)
  Li Luo (1) (2)
  Youmin Wang (1) (2) (4)
  
  1. Institute of Endocrinology & Metabolism, Anhui Medical University, Hefei, People’s Republic of China
  2. Department of Endocrinology, The First Affiliated Hospital of Anhui Medical University, 210 JiXi Road, Hefei, 230032, People’s Republic of China
  4. Anhui Provincial Laboratory of Endocrinology & Metabolism, Anhui Medical University, Hefei, People’s Republic of China
  3. Department of Endocrinology, The First Affiliated Hospital of Anhui University of Traditional Chinese Medicine, Hefei, People’s Republic of China
  
• ISSN：1559-0100

文摘

Fenofibrate is a peroxisome proliferator-activated receptor-α that has been clinically used to treat dyslipidemia and insulin resistance. To better understand the molecular mechanisms underlying fenofibrate action, we investigated whether fenofibrate affects serum levels of vaspin, an adipocytokine that has recently been shown to link obesity and insulin resistance. Fenofibrate treatment significantly increased serum vaspin levels of dyslipidemic patients, which correlated with reduced body weight and increased insulin sensitivity. To elucidate the biochemical mechanisms of fenofibrate action, we investigated the effect of fenofibrate on vaspin mRNA and protein expressions in obese rats. Fenofibrate greatly increased vaspin mRNA and protein levels in visceral adipose tissue consisting of retroperitoneal, mesenteric, and periepididymal adipose tissue but not in the subcutaneous adipose tissue, which correlated with increased serum vaspin levels and increased insulin sensitivity in obese rats. Consistent with a direct effect on vaspin expression, fenofibrate treatment significantly increased the mRNA and protein expression levels of vaspin in 3T3-L1 adipocytes. Together, our results demonstrate for the first time that fenofibrate upregulates vaspin expression in dyslipidemic human subjects and suggest that upregulation of vaspin expression in adipocytes may provide a mechanism by which fenofibrate improves insulin sensitivity in dyslipidemic patients.