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Nutr Metab Cardiovasc Dis. 2014 Jan;24(1):50-6. doi: 10.1016/j.numecd.2013.04.015. Epub 2013 Jun 19.

Plasma adiponectin in heart failure with and without cachexia: catabolic signal linking catabolism, symptomatic status, and prognosis.

Author information

  • 1Applied Cachexia Research, Department of Cardiology, Charite Universitätsmedizin Berlin, Germany.
  • 2Centre for Stroke Research Berlin, Charite Universitätsmedizin Berlin, Germany.
  • 3Division of Cardiology, University Clinic, Golnik, Slovenia.
  • 4Department of Heart Diseases, Wroclaw Medical University, Wroclaw, Poland.
  • 5Department of Endocrinology, Diabetes, and Nutritional Medicine, Universitätsmedizin Berlin, Germany.
  • 6Centre for Clinical and Basic Research, IRCCS San Raffaele, Rome, Italy.
  • 7Department of Endocrinology and Internal Medicine & the Medical Research Laboratories, Department of Clinical Medicine, Aarhus University, Aarhus, Denmark.
  • 8Applied Cachexia Research, Department of Cardiology, Charite Universitätsmedizin Berlin, Germany; Centre for Stroke Research Berlin, Charite Universitätsmedizin Berlin, Germany. Electronic address:



Adiponectin (ADPN) as an adipose tissue hormone contributes to regulation of energy metabolism and body composition and is associated with cardiovascular risk profile parameters. Cardiac cachexia may develop as a result of severe catabolic derangement in chronic heart failure (CHF). We aimed to determinate an abnormal ADPN regulation as a link between catabolic signalling, symptomatic deterioration and poor prognosis.


We measured plasma ADPN in 111 CHF patients (age 65 ± 11, 90% male, left ventricular ejection fraction (LVEF) 36 ± 11%, peak oxygen consumption (peakVO2) 18.1 ± 5.7 l/kg*min, body mass index (BMI) 27 ± 4 kg/m(2), all mean ± standard deviation) and 36 healthy controls of similar age and BMI. Body composition was assessed by dual energy X-ray absorptiometry, insulin sensitivity was evaluated by homoeostasis model assessment, exercise capacity by spiroergometry. Plasma ADPN did not differ between CHF vs. controls (13.5 ± 11.0 vs. 10.5 ± 5.3 mg/l, p > 0.4), but increased stepwise with NYHA functional class (I/II/III: 5.7 ± 1.4/10.7 ± 8.3/19.2 ± 14.0 mg/l, ANOVA p < 0.01). Furthermore, ADPN correlated with VO2 at anaerobic threshold (r = -0.34, p < 0.05). ADPN was highest in cachectic patients (cCHF, 16%) vs. non-cachectic (ncCHF) (18.7 ± 15.0 vs. 12.5 ± 9.9 mg/l; p < 0.05). ADPN indicated mortality risk independently of established prognosticators (HR: 1.04 95% CI: 1.02-1.07; p < 0.0001). ADPN above the mean (13.5 mg/l) was associated with a 3.4 times higher mortality risk in CHF vs. patients with ADPN levels below the mean.


Circulating ADPN is abnormally regulated in CHF. ADPN may be involved in impaired metabolic signalling linking disease progression, tissue wasting, and poor outcome in CHF.

Copyright © 2013 Elsevier B.V. All rights reserved.


Adiponectin; Cachexia; Chronic heart failure; Metabolism

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