Cardioprotective Properties of omentin-1 in Type 2 Diabetes: Evidence From Clinical and in Vitro Studies

PLoS One. 2013;8(3):e59697. doi: 10.1371/journal.pone.0059697. Epub 2013 Mar 29.


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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipose Tissue / drug effects
  • Adipose Tissue / metabolism
  • Aged
  • Animals
  • Case-Control Studies
  • Cytokines / blood
  • Cytokines / metabolism*
  • Cytokines / pharmacology
  • Diabetes Mellitus, Type 2 / metabolism*
  • Diabetes Mellitus, Type 2 / pathology
  • Diabetes Mellitus, Type 2 / physiopathology
  • GPI-Linked Proteins / blood
  • GPI-Linked Proteins / metabolism
  • GPI-Linked Proteins / pharmacology
  • Gene Expression Regulation / drug effects
  • Humans
  • Insulin / metabolism
  • Lectins / blood
  • Lectins / metabolism*
  • Lectins / pharmacology
  • Male
  • Middle Aged
  • Muscle Contraction / drug effects
  • Myocytes, Cardiac / drug effects
  • Myocytes, Cardiac / metabolism*
  • Pioglitazone
  • Rats
  • Signal Transduction / drug effects
  • Thiazolidinediones / pharmacology


  • Cytokines
  • GPI-Linked Proteins
  • ITLN1 protein, human
  • Insulin
  • Lectins
  • Thiazolidinediones
  • Pioglitazone

Grant support

This work was supported by the Federal Ministry of Health, the Ministry of Innovation, Science, Research and Technology of the German State of North Rhine Westphalia, the Commission of the European Communities (Collaborative Project ADAPT, contract no. HEALTH F2-2008-201100), and the German Centre for Diabetes Research (Deutsches Zentrum für Diabetesforschung, DZD). The PIRAMID study (an investigator-initiated study) was supported by Eli Lilly and Company, The Netherlands. The funders had no role in study design, data collection and analysis, or preparation of the manuscript.