Cardioprotective properties of omentin-1 in type 2 diabetes: evidence from clinical and in vitro studies

Sabrina Greulich, Weena J. Y. Chen, Bujar Maxhera, Luuk J. Rijzewijk, Rutger W. van der Meer, Jacqueline T. Jonker, Heidi Mueller, Daniella Herzfeld de Wiza, Ralf-Ruediger Floerke, Konstantinos Smiris, Hildo J. Lamb, Albert de Roos, Jeroen J. Bax, Johannes A. Romijn, Jan W. A. Smit, Payam Akhyari, Artur Lichtenberg, Juergen Eckel, Michaela Diamant, D. Margriet Ouwens

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Abstract

Adipokines are linked to the development of cardiovascular dysfunction in type 2 diabetes (DM2). In DM2-patients, circulating levels of omentin-1, an adipokine preferentially expressed in epicardial adipose tissue, are decreased. This study investigated whether omentin-1 has a cardioprotective function. Omentin-1 levels in plasma and cardiac fat depots were determined in DM2-patients versus controls. Moreover, the relation between omentin-1 levels and cardiac function was examined in men with uncomplicated DM2. Finally, we determined whether omentin-1 could reverse the induction of cardiomyocyte dysfunction by conditioned media derived from epicardial adipose tissue from patients with DM2. Omentin-1 was highly expressed and secreted by epicardial adipose tissue, and reduced in DM2. Circulating omentin-1 levels were lower in DM2 versus controls, and positively correlated with the diastolic parameters early peak filling rate, early deceleration peak and early deceleration mean (all P <0.05). The improved diastolic function following pioglitazone treatment associated with increases in omentin-1 levels (P <0.05). In vitro, exposure of cardiomyocytes to conditioned media derived from epicardial adipose tissue from patients with DM2 induced contractile dysfunction and insulin resistance, which was prevented by the addition of recombinant omentin. These data identify omentin-1 as a cardioprotective adipokine, and indicate that decreases in omentin-1 levels could contribute to the induction of cardiovascular dysfunction in DM2
Original languageEnglish
Article numbere59697
Pages (from-to)e59697
JournalPLOS ONE
Volume8
Issue number3
DOIs
Publication statusPublished - 2013

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