Peripheral, But Not Central, Administration of Adiponectin Reduces Visceral Adiposity and Upregulates the Expression of Uncoupling Protein in Agouti Yellow (<i>Ay/a</i>) Obese Mice

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  • Takayuki Masaki
    Department of Internal Medicine, School of Medicine, Oita Medical University, Oita, Japan
  • Seiichi Chiba
    Department of Internal Medicine, School of Medicine, Oita Medical University, Oita, Japan
  • Tohru Yasuda
    Department of Internal Medicine, School of Medicine, Oita Medical University, Oita, Japan
  • Tetsuo Tsubone
    Department of Internal Medicine, School of Medicine, Oita Medical University, Oita, Japan
  • Tetsuya Kakuma
    Department of Internal Medicine, School of Medicine, Oita Medical University, Oita, Japan
  • Iichiro Shimomura
    Department of Medicine and Pathophysiology, Graduate School of Medicine, Osaka University, Osaka, Japan
  • Tohru Funahashi
    Department of Internal Medicine, Graduate School of Medicine, Osaka University, Osaka, Japan
  • Yuji Matsuzawa
    Department of Internal Medicine, Graduate School of Medicine, Osaka University, Osaka, Japan
  • Hironobu Yoshimatsu
    Department of Internal Medicine, School of Medicine, Oita Medical University, Oita, Japan

Description

<jats:p>To examine the peripheral and central roles of adiponectin in energy intake and expenditure, we investigated the effects of adiponectin on food intake, adiposity, sympathetic nerve activity (SNA), and mRNA expressions of uncoupling protein (UCP) in the brown adipose tissue (BAT), white adipose tissue (WAT) and skeletal muscle in agouti yellow (Ay/a) obese mice. Intraperitoneal administration of adiponectin (1.5 mg/kg for 7 days) attenuated body weight gain and reduced visceral adiposity in Ay/a obese mice compared with PBS-treated controls. In addition, adiponectin treatment increased the expression of UCP1 mRNA in BAT, UCP2 mRNA in WAT, and UCP3 mRNA in skeletal muscle compared with PBS-treated Ay/a controls. Acute peripheral administration of adiponectin (1.5 mg/kg, one injection) also increased SNA in the BAT accompanied by an increase in rectal temperature. Finally, these above responses as well as expression of c-Fos–like immunohistochemistry in the hypothalamus were not induced by central application of adiponectin (0–15 μg/kg). Taken together, adiponectin effectively regulated visceral adiposity, SNA, and UCP mRNA expression peripherally, suggesting that this substance can be used as a therapeutic tool, administered peripherally, in the treatment of visceral obesity and related metabolic disorders.</jats:p>

Journal

  • Diabetes

    Diabetes 52 (9), 2266-2273, 2003-09-01

    American Diabetes Association

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