1. ^*Department of Laboratory Medicine and Pathology, School of Public Health, University of Minnesota, Minneapolis, Minnesota
2. ^‡Division of Epidemiology, School of Public Health, University of Minnesota, Minneapolis, Minnesota
3. ^†Department of Preventative Medicine, School of Medicine, Kyungpook National University, Daegu, Korea
4. ^§Department of Nutrition, University of Oslo, Oslo, Norway

Correspondence: Michael W. Steffes University of Minnesota, Department of Laboratory Medicine and Pathology, MMC 609, 420 Delaware Street S.E., Minneapolis, MN 55454. E-mail: steff001@umn.edu

^*The costs of publication of this article were defrayed, in part, by the payment of page charges. This article must, therefore, be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Received 26 April 2005; Accepted 22 November 2005.

Abstract

Objective: Adiponectin is a collagen-like product of visceral fat that offers apparent protection against macrovascular disease. We evaluated the relationships of concentrations of adiponectin with oxidative stress and the major risk factors for and/or the presence of macrovascular disease.

Research Methods and Procedures: Adiponectin was measured by radioimmunoassay in serum from 3045 fasting participants (ages 33 to 45) of the Coronary Artery Risk Development in Young Adults Study. Cross-sectional correlation of the concentrations of adiponectin with F₂-isoprostane concentrations (a marker of systemic oxidative damage), coronary artery calcification (CAC; an estimate of early macrovascular disease), and several macrovascular risk factors was analyzed.

Results: F₂-isoprostanes and CAC were unrelated to adiponectin after minimal adjustment for gender, race, and center. After additional adjustment for insulin resistance and waist circumference and other macrovascular risk factors, adiponectin correlated positively with high-density lipoprotein-cholesterol (p < 0.0001), F₂-isoprostanes (p < 0.0001), and CAC (less strongly, p < 0.01) and negatively with triglycerides (p < 0.0001) and C-reactive protein (marking inflammation, p = 0.01).

Discussion: Although these data are consistent with reduced cardiovascular disease risk imparted by adiponectin, the higher circulating levels of adiponectin present with oxidative stress and CAC (adjusting for waist and insulin resistance) may indicate an enhanced adiponectin secretory response of adipose tissue to the metabolic environment present in the early development of macrovascular disease. Thus, the elevated levels of adiponectin may comprise an attempt to alleviate risk for additional development and progression of macrovascular disease in an at-risk environment.