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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 《PloS one》2013,8(3)
Context
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.Methods
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.Results
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.Conclusion
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. 相似文献2.
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