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Comparative Study
. 2013 Jan;124(2):115-22.
doi: 10.1042/CS20120004.

Circulating adipocyte fatty acid-binding protein levels are independently associated with heart failure

Mingya Liu  1 , Mi Zhou, Yuqian Bao, Zhiyong Xu, Huating Li, Hao Zhang, Wei Zhu, Jialiang Zhang, Aimin Xu, Meng Wei, Weiping Jia
Affiliations
Comparative Study

Circulating adipocyte fatty acid-binding protein levels are independently associated with heart failure

Mingya Liu et al. Clin Sci (Lond). 2013 Jan.

Abstract

A-FABP (adipocyte fatty acid-binding protein), one of the most abundant proteins in adipocytes, plays a key role in obesity-related insulin resistance, inflammation and atherosclerosis in animals. In the present study, we sought to investigate the association of A-FABP with HF (heart failure) in Chinese subjects. Serum A-FABP levels were measured in 252 HF patients and 261 age-, gender- and BMI (body mass index)-matched non-HF subjects. Echocardiography was performed on each patient. The severity of HF was determined by the NYHA (New York Heart Association) classification system. After adjustments for age, gender and BMI, serum A-FABP concentrations in patients with HF were significantly higher than in non-HF patients [11.17 (6.63-19.93) ng/ml compared with 5.67 (3.20-8.87) ng/ml; P<0.001] and significantly progressed with the NYHA class (P<0.001). In addition, NT-proBNP (N-terminal pro-brain natriuretic peptide) was independently and positively correlated with A-FABP (standardized β=0.340, P<0.001) after adjusting for confounding factors. Each echocardiographic parameter, especially LVEF (left ventricular ejection fraction), was independently associated with A-FABP (all P<0.05). Multivariate logistic regression analysis demonstrated that A-FABP concentration was an independent risk factor for HF [odds ratio, 6.93 (95% confidence interval, 2.49-19.30); P<0.001]. Our results demonstrate that A-FABP is closely associated with HF, and raise the possibility that increased A-FABP may be causally related to the pathogenesis of heart dysfunction in humans.

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