Serum fetuin-A and arginase-1 in human obesity model: Is there any interaction between inflammatory status and arginine metabolism?

Abstract

Obesity is a major risk factor for many chronic metabolic diseases such as inflammation, insulin resistance (IR) and fatty liver injury. It was reported that obesity causes some variations on the serum levels of fetuin-A and is associated with arginine metabolism, especially arginase-1 levels. The aim of our study was to evaluate, the interaction and possible changes of these liver over produced proteins, fetuin-A and arginase-1 levels in obesity-related inflammatory status. Study groups were composed of individuals aged between 19 and 63 (n = 62). The control group included healthy subjects with BMI < 25, obese group included obese patients with BMI > 30 and with no other chronic disease. Biochemical markers were determined by an auto-analyzer. Adiponectin, fetuin-A, arginase-1, asymmetric dimethylarginine (ADMA), arginine, Hexanoyl-lysine (HEL) and leptin levels were measured with commercial ELISA immunoassay kits. Nitrite and nitrate were determined with colorimetric assay kit in serum samples. High sensitive C-reactive protein (hsCRP) levels and liver function enzymes activities were higher in the obese group in respect to the control group. Serum fetuin-A, arginase-1 and leptin levels were increased but adiponectin levels were decreased in obese subjects. Fetuin-A levels showed significant correlations with arginase-1 and HOMA-IR. Consequently, we carried out an investigation about higher serum fetuin-A and arginase-1 levels may have an important role in obesity and obesity-related liver damage.

Key Words::

• α2-Heremans Schmid glycoprotein
• adiponectin
• insulin resistance
• C-reactive protein (CRP)
• leptin

Acknowledgements

This study was supported by the Research Funds of Istanbul Bilim University (201301-11). The authors thank Omer Uysal, PhD, Department of Public Health, for his contribution to the statistical analyses.

Declaration of interest: The authors report no conflict of interest. The authors alone are responsible for the content and writing of the paper.