Osteoprotegerin increases parallel to insulin resistance in obese adolescents

ABSTRACT

Purpose/Aim of the Study: Osteoprotegerin (OPG) is an α tumor necrosis factor receptor superfamily glucoprotein that acts as a decoy receptor for the receptor activator of nuclear factor kappa B ligand (RANKL), exerting an antiresoptive bone effect. It was recently shown that OPG/RANKL axis is activated during vascular calcification, contributing to atherosclerotic lesions formation. Additionally, OPG levels are charachterized as an independent risk factor for overall vascular mortality in obese adults. We aimed to investigate OPG levels in children/adolescents with obesity and explore possible relations with obesity-related insulin resistance (IR). Material and Methods: A total of 160 participants (85 obese) were enrolled. Participants with obesity underwent an oral glucose tolerance test. IR was evaluated according to the homeostasis model assessment-insulin resistance index. Serum OPG levels were determined. Results: OPG levels did not differ significantly between obese subjects and controls in the total sample (p = 0.133). However, in the adolescents’ subgroup, serum OPG levels were significantly increased in obesity (p = 0.019). After stratifying participants according to their IR status, only subjects with both obesity and IR exhibited increased OPG levels compared to controls (p < 0.001). Factor analysis further associated OPG levels variation to insulin levels variation and to IR. Conclusions: Obese individuals demonstrate increased serum OPG levels during puberty. Obesity per se is not the potent factor for this increase; indeed, IR accompanying obesity seems to exert a fundamental role in OPG upregulation.

KEYWORDS:

• Adolescents
• children
• insulin resistance
• obesity
• οsteoprotegerin

Acknowledgments

Part of this study was presented at the 55th Annual ESPE Annual Meeting on 10–12th September 2016, in Paris, France.

Declaration of interest

The study was supported by the Research Committee of the Aristotle University of Thessaloniki (project code: 83022). The Aristotle University Research Committee played no role in the study design, collection, analysis and interpretation of data, writing of the report. All authors report no conflict of interest.

Additional information

Funding

This work was supported by the Research Committee, Aristotle University of Thessaloniki [Research in pediatric diabetes, 83022].