Discrimination Between Obesity and Insulin Resistance in the Relationship With Adiponectin

  1. Fahim Abbasi1,
  2. James W. Chu1,
  3. Cindy Lamendola1,
  4. Tracey McLaughlin1,
  5. John Hayden2,
  6. Gerald M. Reaven1 and
  7. Peter D. Reaven2
  1. 1Divisions of Cardiovascular Medicine and Endocrinology and Metabolism, Department of Medicine, Stanford University School of Medicine, Stanford, California
  2. 2Division of Endocrinology and Metabolism, Department of Medicine, Carl T. Hayden Veterans Affairs Medical Center, Phoenix, Arizona
  1. Address correspondence reprint requests to Peter Reaven MD, Division of EndocrinologyMetabolism, Department of Medicine (CS-111E), Carl T. Hayden Veterans Affairs Medical Center, 650 East Indian School Rd., Phoenix, AZ 85012. E-mail: peter.reaven{at}med.va.gov

Abstract

Insulin resistance and obesity are both associated with lower plasma adiponectin concentrations. Since insulin resistance and obesity are related, the extent to which the association of adiponectin with insulin resistance is dependent on its relationship with obesity is unclear. To address this issue, fasting plasma adiponectin concentrations were measured in 60 nondiabetic subjects, stratified into four equal groups on the basis of both their degree of adiposity and insulin resistance. Insulin resistance was quantified by determining the steady-state plasma glucose (SSPG) concentration in response to an infusion of octreotide, glucose, and insulin, and degree of adiposity was assessed by BMI. Subjects were defined as obese (BMI ≥30.0 kg/m2) or nonobese (<27.0 kg/m2) and as either insulin sensitive (SSPG <100 mg/dl) or insulin resistant (>190 mg/dl). Insulin-resistant subjects had significantly (P<0.001) lower (mean ± SD) adiponectin concentrations, whether they were obese (17.1 ± 5.9 μg/ml) or nonobese (16.3 ± 7.5 μg/ml) as compared with either obese, insulin-sensitive (34.3 ± 13.1 μg/ml) or nonobese, insulin-sensitive (29.8 ± 15.3 μg/ml) subjects. Finally, adiponectin levels in insulin-sensitive subjects varied to a significantly greater degree than in insulin-resistant subjects. These results suggest that adiponectin concentrations are more closely related to differences in insulin-mediated glucose disposal than obesity.

Footnotes

    • Accepted December 15, 2003.
    • Received June 30, 2003.
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