Abstract 13125: Circulating Levels of Novel Adipokines and Their Association with Vascular Function in the Community: The Framingham Third Generation Cohort
Background: Adipose tissue is thought to be a critical regulator of vascular function and recent work has focused on the potential vascular effects of mediators secreted from fat depots (adipokines). Retinol binding protein-4 (RBP4), adipocyte-fatty acid binding protein (A-FABP), adiponectin, leptin and leptin-receptor (LEP-R) are adipokines that mediate metabolic dysregulation and vascular dysfunction.
Methods: We examined the cross-sectional association of 5 circulating adipokines with mean arterial pressure (MAP) and carotid-femoral pulse wave velocity (CFPWV), as measured by arterial tonometry, in 3388 participants free of CVD in the Framingham 3rd generation cohort (mean age 40 years, 53% female). Separate regression models were used to examine the relations of each adipokine to MAP and CFPWV adjusting for age, sex, heart rate, height, antihypertensive treatment, total and HDL cholesterol, smoking and diabetes (CFPWV analyses also included MAP).
Results: Mean adipokine levels were 40.7 ± 10.7 ng/ml for RBP-4, 18.6 ± 10.3 ng/ml for A-FABP, 11.4 ± 12.9 ng/ml for leptin, 19.6 ± 8.6 ng/ml for LEP-R, and 8.7 ± 5.5 ng/ml for adiponectin. The mean MAP was 89.1 ± 10.8 mm Hg and mean CFPWV was 7.0 ± 1.3 m/s. Levels of RBP-4, A-FABP and leptin were positively associated with MAP (P<0.001 for all); adiponectin was inversely related to MAP (P=0.003). RBP-4 and A-FABP were positively associated with CFPWV, while LEP-R was inversely related to CFPWV (P<0.05 for all); relations with CFPWV persisted after further adjustment for weight.
Conclusions: In our cross-sectional, community-based study of healthy middle-age adults, a pattern of higher levels of A-FABP and RBP4 and lower levels of LEP-R, was associated with arterial stiffness after accounting for relations with MAP. These findings are consistent with the hypothesis that adipokines regulate vascular homeostasis and may help elucidate mechanisms by which excess adiposity contributes to vascular dysfunction.
- © 2011 by American Heart Association, Inc.