Mary J Christoph1, Matthew A Allison2, James S Pankow3, Paul A Decker4, Phillip S Kirsch4, Michael Y Tsai5, Michele M Sale6, Mariza de Andrade4, Hugues Sicotte4, Weihong Tang3, Naomi Q Hanson5, Cecilia Berardi4,7, Christina L Wassel8, Nicholas B Larson4, Suzette J Bielinski4. 1. Department of Kinesiology and Community Health, University of Illinois at Urbana-Champaign, Urbana, Illinois, USA. 2. Department of Family and Preventive Medicine, University of California, San Diego, La Jolla, California, USA. 3. Division of Epidemiology and Community Health, University of Minnesota, Minneapolis, Minnesota, USA. 4. Division of Epidemiology, Department of Health Sciences Research, Mayo Clinic, Rochester, Minnesota, USA. 5. Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, Minnesota, USA. 6. Center for Public Health Genomics, University of Virginia, Charlottesville, Virginia, USA. 7. Montefiore Medical Center, Bronx, New York, USA. 8. Department of Epidemiology, University of Pittsburgh, Pennsylvania, USA.
Abstract
OBJECTIVE: At the cellular level, how excess adiposity promotes atherogenesis is not fully understood. One pathway involves secretion of adipokines that stimulate endothelial dysfunction through increased expression of adhesion molecules. However, the relationship of adiposity to adhesion molecules that promote atherosclerosis is largely unknown. METHODS: Linear regression models were used to assess the sex-specific associations of soluble cellular adhesion molecules (sP- and sL-selectin, sICAM-1, sVCAM-1, and sHGF) and adiposity in 5,974 adults examined as part of the Multi-Ethnic Study of Atherosclerosis (MESA). Adiposity measures included body mass index (BMI), waist-to-hip-ratio (WHR), and computed tomography measures of subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT). RESULTS: The mean age was 64 years and 52% were female. In multivariable models adjusting for traditional cardiovascular risk factors, sHGF was positively associated with BMI, WHR, and VAT in both males and females, and sP-selectin with WHR and VAT in males. sVCAM-1 was inversely associated with VAT in females only. CONCLUSIONS: Our results showed the relation of adiposity to soluble cellular adhesion proteins was similar across adiposity measures and for both sexes. However, the relationship between adiposity and sVCAM-1 and P-selectin may be modified by sex and the measure used to assess adiposity.
OBJECTIVE: At the cellular level, how excess adiposity promotes atherogenesis is not fully understood. One pathway involves secretion of adipokines that stimulate endothelial dysfunction through increased expression of adhesion molecules. However, the relationship of adiposity to adhesion molecules that promote atherosclerosis is largely unknown. METHODS: Linear regression models were used to assess the sex-specific associations of soluble cellular adhesion molecules (sP- and sL-selectin, sICAM-1, sVCAM-1, and sHGF) and adiposity in 5,974 adults examined as part of the Multi-Ethnic Study of Atherosclerosis (MESA). Adiposity measures included body mass index (BMI), waist-to-hip-ratio (WHR), and computed tomography measures of subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT). RESULTS: The mean age was 64 years and 52% were female. In multivariable models adjusting for traditional cardiovascular risk factors, sHGF was positively associated with BMI, WHR, and VAT in both males and females, and sP-selectin with WHR and VAT in males. sVCAM-1 was inversely associated with VAT in females only. CONCLUSIONS: Our results showed the relation of adiposity to soluble cellular adhesion proteins was similar across adiposity measures and for both sexes. However, the relationship between adiposity and sVCAM-1 and P-selectin may be modified by sex and the measure used to assess adiposity.
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