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Adiponectin, diabetes and ischemic heart failure: a challenging relationship

Samuele Baldasseroni12*, Alessandro Antenore12, Claudia Di Serio12, Francesco Orso12, Giuseppe Lonetto12, Nadia Bartoli12, Alice Foschini12, Andrea Marella12, Alessandra Pratesi12, Salvatore Scarantino12, Stefano Fumagalli12, Matteo Monami12, Edoardo Mannucci12, Niccolò Marchionni12 and Francesca Tarantini12

Author Affiliations

1 Department of Critical Care Medicine and Surgery, Geriatric Medicine Unit, University of Florence, Florence, Italy

2 Department of Heart and Vessels, Geriatric Cardiology and Medicine Unit, University of Florence and Azienda Ospedaliero-Universitaria Careggi [AOUC], Viale Morgagni 85, 50134, Florence, Italy

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Cardiovascular Diabetology 2012, 11:151  doi:10.1186/1475-2840-11-151

Published: 18 December 2012



Several peptides, named adipokines, are produced by the adipose tissue. Among those, adiponectin (AD) is the most abundant. AD promotes peripheral insulin sensitivity, inhibits liver gluconeogenesis and displays anti-atherogenic and anti-inflammatory properties. Lower levels of AD are related to a higher risk of myocardial infarction and a worse prognosis in patients with coronary artery disease. However, despite a favorable clinical profile, AD increases in relation to worsening heart failure (HF); in this context, higher adiponectinemia is reliably related to poor prognosis. There is still little knowledge about how certain metabolic conditions, such as diabetes mellitus, modulate the relationship between AD and HF.

We evaluated the level of adiponectin in patients with ischemic HF, with and without type 2 diabetes, to elucidate whether the metabolic syndrome was able to influence the relationship between AD and HF.


We demonstrated that AD rises in patients with advanced HF, but to a lesser extent in diabetics than in non-diabetics. Diabetic patients with reduced systolic performance orchestrated a slower rise of AD which began only in face of overt HF. The different behavior of AD in the presence of diabetes was not entirely explained by differences in body mass index. In addition, NT-proBNP, the second strongest predictor of AD, did not differ significantly between diabetic and non-diabetic patients. These data indicate that some other mechanisms are involved in the regulation of AD in patients with type 2 diabetes and coronary artery disease.


AD rises across chronic heart failure stages but this phenomenon is less evident in type 2 diabetic patients. In the presence of diabetes, the progressive increase of AD in relation to the severity of LV dysfunction is hampered and becomes evident only in overt HF.

Adiponectin; Diabetes; Coronary artery disease; Heart failure