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Relations of Circulating Resistin and Adiponectin and Cardiac Structure and Function: The Framingham Offspring Study
Author(s) -
McManus David D.,
Lyass Asya,
Ingelsson Erik,
Massaro Joseph M.,
Meigs James B.,
Aragam Jayashri,
Benjamin Emelia J.,
Vasan Ramachandran S.
Publication year - 2012
Publication title -
obesity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.438
H-Index - 199
eISSN - 1930-739X
pISSN - 1930-7381
DOI - 10.1038/oby.2011.32
Subject(s) - adiponectin , resistin , medicine , adipokine , framingham heart study , quartile , endocrinology , framingham risk score , cardiology , offspring , ventricular remodeling , heart failure , obesity , disease , pregnancy , insulin resistance , confidence interval , biology , genetics
Obesity is associated with pathological cardiac remodeling and risk of heart failure (HF). Adipocytokines (ADKs) may mediate the increased risk of cardiovascular disease associated with excess adiposity. Yet data relating ADKs to cardiac remodeling phenotypes are sparse. We related two circulating ADKs, resistin and adiponectin, to three important echocardiographic markers of cardiac remodeling, left ventricular mass (LVM), left atrial diameter (LAD), and LV fractional shortening (LVFS) in 2,615 participants (mean age 61 years, 55% women) in the Framingham Offspring Study. Adiponectin concentrations were inversely related to LVM in multivariable linear regression models adjusting for key clinical correlates including BMI (regression coefficient per s.d.‐increment in ln‐adiponectin = −3.37, P = 0.02; P for trend across quartiles = 0.02). Adiponectin was not associated with LAD or LVFS ( P > 0.56). Resistin concentrations were inversely related to LVFS (regression coefficient per s.d.‐increment in ln‐resistin = −0.01, P = 0.03; P for trend across quartiles = 0.04). Resistin was not associated with LVM or LAD ( P > 0.05). In our moderate‐sized, community‐based sample, higher circulating concentrations of adiponectin and resistin were associated with lower LVM and lower LVFS, respectively. In conclusion, these associations identify potential mechanisms by which excess adiposity may mediate adverse cardiac remodeling and HF risk.