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Hepatokines as a Link between Obesity and Cardiovascular Diseases
Hye Jin Yoo, Kyung Mook Choi
Diabetes Metab J. 2015;39(1):10-15.   Published online February 16, 2015
DOI: https://doi.org/10.4093/dmj.2015.39.1.10
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  • 67 Web of Science
  • 69 Crossref
AbstractAbstract PDFPubReader   

Non-alcoholic fatty liver disease, which is considered a hepatic manifestation of metabolic syndrome, independently increases the risks of developing cardiovascular disease (CVD) and type 2 diabetes mellitus. Recent emerging evidence suggests that a group of predominantly liver-derived proteins called hepatokines directly affect the progression of atherosclerosis by modulating endothelial dysfunction and infiltration of inflammatory cells into vessel walls. Here, we summarize the role of the representative hepatokines fibroblast growth factor 21, fetuin-A, and selenoprotein P in the progression of CVD.

Citations

Citations to this article as recorded by  
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Original Article
Serum Visfatin and Fetuin-A Levels and Glycemic Control in Patients with Obese Type 2 Diabetes Mellitus
Fethiye Oztop Gunduz, Sembol Turkmen Yildirmak, Mustafa Temizel, Yilmaz Faki, Mustafa Cakmak, Mustafa Durmuscan, Funda Sezgin
Diabetes Metab J. 2011;35(5):523-528.   Published online October 31, 2011
DOI: https://doi.org/10.4093/dmj.2011.35.5.523
  • 65,535 View
  • 29 Download
  • 10 Crossref
AbstractAbstract PDFPubReader   
Background

Visfatin is an adipokine produced by visceral adipose tissue and has insulin-mimicking effects. Fetuin-A is a hepatic secretory protein that binds the insulin receptor and inhibits insulin action both in vivo and in vitro. The authors of the present study aimed to investigate the levels of serum visfatin and fetuin-A and their correlation with hemoglobin A1c (HbA1c) and urine albumin levels in patients with type 2 diabetes mellitus (T2DM).

Methods

A total of 40 obese patients with T2DM (11 males and 29 females; age, 54.47±10.83 years and 23 obese nondiabetic controls (8 males and 15 females; age, 53.04±11.33 years) were included in the study. Age, sex, and body mass index were similar in the 2 groups. Serum visfatin and fetuin-A levels were measured by enzyme-linked immunosorbent assay. HbA1c and urine albumin levels were measured by high performance liquid chromatography and nephelometric method, respectively.

Results

Serum levels of visfatin in patients with T2DM (4.03±2.44 ng/mL) were similar to the control group (3.65±3.02 ng/mL). Serum fetuin-A levels were significantly lower in patients with T2DM than the controls (298.75±78.86 and 430.73±94.46 µg/mL, respectively). HbA1c levels were significantly higher in the T2DM group compared with controls (7.33±1.32 and 5.44±0.84%, respectively). Correlations between visfatin, fetuin-A and HbA1c levels were not observed.

Conclusion

The present study suggests fetuin-A may play a role in the pathogenesis of T2DM.

Citations

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