Pentraxin-3, Angiopoietin-Like Protein-3, Angiopoietin-Like Protein-4 and Angiopoietin-Like Protein-8 Levels in Morbid Obese Children

A low-grade inflammatory state accompanies obesity and metabolic syndrome (MetS), which are risk factors for cardiovascular diseases (CVD) in children’s future lives. The aim of this study is to investigate possible associations of pentraxin 3 (PTX3), a promising new marker for CVDs, with angiopoietin-like proteins (ANGPTL) in morbid obese (MO) children and their potential uses in the prediagnosis of MetS. Thirty normal weight (NW) and 50 MO prepubertal children without MetS symptoms, a total of 80, participated in the study. Using percentile tables for age and gender recommended by WHO, children whose percentiles were between 15-85 and above 99 were included in NW and MO groups, respectively. Anthropometric measurements, BMI and HOMA-IR values were recorded. Serum PTX3, ANGPTL3, ANGPTL4, ANGPTL8/betatrophin levels were determined by enzymelinked immunosorbent assay (ELISA). Statistical analyses were performed by SPSS. p < 0.05 was the degree of statistical significance. There were no differences between PTX3, ANGPTL3 and ANGPTL4 levels of groups. ANGPTL8/betatrophin levels were significantly higher in MO children (p ≤ 0.001). A significant correlation was observed between PTX3 and ANGPTL4 (r = 0.297, p ≤ 0.05) in the same group. When adjusted for MetS parameters including HDL-Chol, correlations http://mo.qingres.com PTX3, ANGPTL-3, 4, 8 in Obesity Mustafa Metin Donma et al. MED ONE 2017, 2:e170029 | Email:[email protected] December 22, 2017 2 between ANGPTL3-ANGPTL8/betatrophin (r = 0.327, p ≤ 0.05) and PTX3-ANGPTL4 (r = 0.337, p ≤ 0.05) were detected. When HDL-Chol was replaced with TRG these associations were disappeared. This study is the first to perform PTX3, ANGPTL3, ANGPTL4, ANGPTL8/betatrophin measurements in prepubertal NW and MO children. Upon evaluation of dyslipidemia in MetS, adjustment for MetS parameters pointed out HDL-Chol as the more valuable parameter than TRG, based upon the existence of ANGPTL3-ANGPTL8/betatrophin as well as PTX3-ANGPTL4 associations.