Plasma Adiponectin, Insulin Sensitivity, and Subclinical Inflammation in Women With Prior Gestational Diabetes Mellitus

  1. Christine Winzer, MD1,
  2. Oswald Wagner, MD2,
  3. Andreas Festa, MD3,
  4. Barbara Schneider, PHD4,
  5. Michael Roden, MD4,
  6. Dagmar Bancher-Todesca, MD5,
  7. Giovanni Pacini, PHD6,
  8. Tohru Funahashi, MD7 and
  9. Alexandra Kautzky-Willer, MD1
  1. 1Department of Internal Medicine III, Division of Endocrinology and Metabolism, Vienna University Hospital, Vienna, Austria
  2. 2Department of Laboratory Diagnostics, Vienna University Hospital, Vienna, Austria
  3. 3Eli Lilly & Company, Vienna, Austria
  4. 4Institute for Medical Statistics, University of Vienna, Vienna, Austria
  5. 5Department of Gynecology and Obstetrics, University of Vienna, Vienna, Austria
  6. 6Institute of Systems Science and Biomedical Engineering, Metabolic Unit, Italian National Research Council, Padova, Italy
  7. 7Second Department of Internal Medicine, Osaka University Medical School, Osaka, Japan
  1. Address correspondence and reprint requests to A. Kautzky-Willer, MD, Department of Medicine III, Division of EndocrinologyMetabolism, University of Vienna A-1090 Wien, Währinger Gürtel 18-20, Vienna, Austria. E-mail: alexandra.kautzky-willer{at}


OBJECTIVE—Women with prior gestational diabetes mellitus (pGDM) are at increased risk of developing type 2 diabetes and associated vasculopathy. Because increased fat mass and inflammatory processes are angiopathic risk factors, the relationship between insulin sensitivity, parameters of subclinical inflammation, and plasma concentrations of adipocytokines was investigated in pGDM both at 3 months and 12 months after delivery.

RESEARCH DESIGN AND METHODS—Insulin sensitivity (through a frequently sampled intravenous glucose tolerance test) and plasma concentrations of ultrasensitive C-reactive protein (CRP), adiponectin, plasminogen activator inhibitor (PAI)-1, tumor necrosis factor-α, leptin, and interleukin-6 were measured in 89 pGDM (BMI 26.9 ± 0.5 kg/m2, age 32 ± 0.5 years) and in 19 women with normal glucose tolerance during pregnancy (NGT) (23.7 ± 0.9 kg/m2, 31 ± 1.3 years).

RESULTS—pGDM showed lower (P < 0.0001) plasma adiponectin (6.7 ± 0.2 μg/ml) than NGT (9.8 ± 0.6 μg/ml) and a decreased (P < 0.003) insulin sensitivity index (Si) and disposition index (P < 0.03), but increased plasma leptin (P < 0.003), PAI-1 (P < 0.002), and CRP (P < 0.03). After adjustment for body fat mass, plasma adiponectin remained lower in pGDM (P < 0.004) and correlated positively with Si (P < 0.003) and HDL cholesterol (P < 0.0001) but negatively with plasma glucose (2-h oral glucose tolerance test [OGTT]) (P < 0.0001), leptin (P < 0.01), CRP (P < 0.007), and PAI-1 (P < 0.0001). On regression analysis, only HDL cholesterol, postload (2-h OGTT) plasma glucose, and Si remained significant predictors of plasma adiponectin, explaining 42% of its variability. Of note, adiponectin further decreased (P < 0.05) only in insulin-resistant pGDM despite unchanged body fat content and distribution after a 1-year follow-up.

CONCLUSIONS—Lower plasma adiponectin concentrations characterize women with previous GDM independently of the prevailing insulin sensitivity or the degree of obesity and are associated with subclinical inflammation and atherogenic parameters.


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

    • Accepted March 23, 2004.
    • Received January 8, 2004.
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