Abstract

C1q/TNF-Related Protein-3 (CTRP3) and CTRP13 are two newly discovered adipokines regulating glucose and lipid metabolism. But their role in type 2 diabetes mellitus (T2DM) and coronary artery disease (CAD) is still in infancy. The aim of this study was to investigate the associations of gene expression and serum levels of CTRP3 and CTRP13 with CAD, metabolic and inflammatory markers in patients with and without T2DM. Serum levels of CTRP3, CTRP13, adiponectin and inflammatory cytokines and their gene expression in peripheral blood mononuclear cells (PBMCs) were determined in 172 subjects categorized as group I (without T2DM and CAD), group II (with CAD but no T2DM), group III (with T2DM but no CAD) and group IV (with T2DM and CAD). Serum levels and gene expression of CTRP3, CTRP13 and adiponectin in the group I were higher compared to other groups. Inflammatory cytokines in the control group were lower than other groups too. CTRP3 serum levels have an independent association with BMI, smoking and CTRP3 gene expression; also CTRP13 serum levels has an independent association with BMI, HDL-C, insulin, HOMA-IR, HbA1c and TNF-α. Decreased serum levels of CTRP3 and CTRP13 were also associated with CAD. It appears that the decreased levels of CTRP3 and especially CTRP13 were associated with increased risk of T2DM and CAD. These findings suggest an emerging role of these adipokines in the pathogenesis of CAD, but further studies are necessary to establish this concept.

Highlights

  • Adipose tissue is recognized as the largest endocrine organ in the body that secretes various adipokines such as tumor necrosis factor-alpha (TNF-α), resistin, visfatin and leptin [1]

  • There is ample evidence showing plausible role of C1q TNF-related proteins (CTRP) in the pathogenesis of type 2 diabetes mellitus (T2DM) and coronary artery disease (CAD), since the expression of members of this family are dysregulated in metabolic diseases and obesity [24,25,26,27,28]

  • We showed that serum concentration of C1q/TNF-Related Protein-3 (CTRP3) is lower in CAD patients with and without T2DM

Read more

Summary

Introduction

Adipose tissue is recognized as the largest endocrine organ in the body that secretes various adipokines such as tumor necrosis factor-alpha (TNF-α), resistin, visfatin and leptin [1]. Among adipokines secreted from adipose tissue, adiponectin is one of the most potent molecules with respect to anti-atherosclerotic, anti-inflammatory and insulin-sensitizing activities [2,3], adiponectin-deficient animal models display modest phenotype [4]. This discrepancy suggests that a compensatory effect may be caused by the family of C1q TNF-related proteins (CTRP) [4,5]. Despite structural similarities between CTRP family and adiponectin, they exert pleiotropic effects on cell metabolism and have different regulation patterns [6]

Objectives
Methods
Results
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call