Synthetic Peroxisome Proliferator-Activated Receptor-γ Agonist, Rosiglitazone, Increases Plasma Levels of Adiponectin in Type 2 Diabetic Patients

  1. Wei-Shiung Yang, MD, PHD12,
  2. Chi-Yuan Jeng, MD, PHD3,
  3. Ta-Jen Wu, MD, PHD4,
  4. Sachiyo Tanaka, MD, PHD5,
  5. Tohru Funahashi, MD, PHD5,
  6. Yuji Matsuzawa, MD, PHD5,
  7. Jao-Ping Wang, BS1,
  8. Chi-Ling Chen, PHD6,
  9. Tong-Yuan Tai, MD, PHD1 and
  10. Lee-Ming Chuang, MD, PHD12
  1. 1Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan
  2. 2Graduate Institute of Clinical Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan
  3. 3Department of Internal Medicine, Tri-Service General Hospital, Taipei, Taiwan
  4. 4Department of Internal Medicine, National Cheng-Kung University Hospital, Tainan, Taiwan
  5. 5Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, Osaka, Japan
  6. 6Institute of Epidemiology, College of Public Health, National Taiwan University, Taipei, Taiwan


    OBJECTIVE—Adiponectin, a plasma protein exclusively synthesized and secreted by adipose tissue, has recently been shown to have anti-inflammatory, antiatherogenic properties in vitro and beneficial metabolic effects in animals. Lower plasma levels of adiponectin have been documented in human subjects with metabolic syndrome and coronary artery disease. We investigated whether the level of this putative protective adipocytokine could be increased by treatment with a peroxisome proliferator-activated receptor-γ (PPAR-γ) agonist in diabetic patients.

    RESEARCH DESIGN AND METHODS—Type 2 diabetic patients (30 in the treatment group and 34 in the placebo group) were recruited for a randomized double-blind placebo-controlled trial for 6 months with the PPAR-γ agonist rosiglitazone. Blood samples were collected and metabolic variables and adiponectin levels were determined in all patients before initiation of the study.

    RESULTS—In the rosiglitazone group, mean plasma adiponectin level was increased by more than twofold (P < 0.0005), whereas no change was observed in the placebo group. Multivariate linear regression analysis showed that whether rosiglitazone was used was the single variable significantly related to the changes of plasma adiponectin. The amount of variance in changes of plasma adiponectin level explained by the treatment was ∼24% (r2 = 0.24) after adjusting for age, sex, and changes in fasting plasma glucose, HbA1c, insulin resistance index, and BMI.

    CONCLUSIONS—Rosiglitazone increases plasma adiponectin levels in type 2 diabetic subjects. Whether this may contribute to the antihyperglycemic and putative antiatherogenic benefits of PPAR-γ agonists in type 2 diabetic patients warrants further investigation.


    • Address correspondence and reprint requests to Lee-Ming Chuang, MD, PhD, Department of Internal Medicine, National Taiwan University Hospital, 7 Chung-Shan South Road, Taipei, Taiwan. E-mail: leeming{at}

      Received for publication 20 June 2001 and accepted in revised form 24 October 2001.

      L.M.C. has received funding from Smith-Kline Beecham.

      A table elsewhere in this issue shows conventional and Système International (SI) units and conversion factors for many substances.

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