Abstract: Iron is physiologically essential. However, it also participates in the catalysis of free radical formation reactions. Its deficiency is associated with amplified health risks. This trace element establishes some links with another physiological process related to cell death, apoptosis. Both iron deficiency and iron overload are closely associated with apoptosis. Soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) has the ability to trigger apoptosis and plays a dual role in the physiological versus pathological inflammatory responses of tissues. The aim of this study was to investigate the status of these parameters as well as the associations among them in children with obesity, a low-grade inflammatory state. The study was performed on groups of children with normal body mass index (N-BMI) and obesity. 43 children were included in each group. Based upon age- and sex-adjusted BMI percentile tables prepared by the World Health Organization, children whose values varied between 85 and 15 were included in N-BMI group. Children, whose BMI percentile values were between 99 and 95, comprised obese (OB) group. Institutional ethical committee approval and informed consent forms were taken prior to the study. Anthropometric measurements (weight, height, waist circumference, hip circumference, head circumference, neck circumference) and blood pressure values (systolic blood pressure and diastolic blood pressure) were recorded. Routine biochemical analyses, including serum iron, total iron binding capacity (TIBC), transferrin saturation percent (Tf Sat %) and ferritin, were performed. sTWEAK levels were determined by enzyme-linked immunosorbent assay. study data were evaluated using appropriate statistical tests performed by the statistical program SPSS. Serum iron levels were 91 ± 34 mcrg/dl and 75 ± 31 mcrg/dl in N-BMI and OB children, respectively. The corresponding values for TIBC, Tf Sat %, ferritin were 265 mcrg/dl vs. 299 mcrg/dl, 37.2 ± 19.1% vs. 26.7 ± 14.6%, and 41 ± 25 ng/ml vs 44 ± 26 ng/ml. In N-BMI and OB groups, sTWEAK concentrations were measured as 351 ng/L and 325 ng/L, respectively (p > 0.05). Correlation analysis revealed significant associations between sTWEAK levels and iron related parameters (p < 0.05) except ferritin. In conclusion, iron contributes to apoptosis. Children with iron deficiency have decreased apoptosis rate in comparison with that of healthy children. sTWEAK is an inducer of apoptosis. OB children had lower levels of both iron and sTWEAK. Low levels of sTWEAK are associated with several types of cancers and poor survival. Although iron deficiency state was not observed in this study, the correlations detected between decreased sTWEAK and decreased iron as well as Tf Sat % values were valuable findings, which point out decreased apoptosis. This may induce a proinflammatory state, potentially leading to malignancies in the future lives of OB children.
Abstract: Obesity, as excessive fat accumulation in the body, is a global health problem. The prevalence of obesity and its complications increase due to easy access to high-energy food and decreased physical activity. Cardiovascular diseases (CVDs) constitute a significant part of obesity-related morbidity and mortality. Since the effects of obesity on cardiovascular system may start during childhood without clinical findings, elucidating the mechanisms of cardiovascular changes associated with childhood obesity became more important. In this study, we aimed to investigate some biochemical parameters which may be involved in obesity-related pathologic processes of CVDs. One hundred and seventy-seven children were included in the study, and they were divided into four groups based upon WHO criteria and presence of the metabolic syndrome (MetS): children with normal-BMI, obesity, morbid obesity, and MetS. High-sensitive cardiac troponin T (hs-cTnT), cardiac myosin binding protein C (cMyBP-C), trimethylamine N-oxide (TMAO), soluble tumor necrosis factor-like weak inducer (sTWEAK), chromogranin A (CgA), multimerin-2 levels, and other biochemical parameters were measured in serum samples. Anthropometric measurements and clinical findings of the children were recorded. Statistical analyses were performed. Children with normal-BMI had significantly higher CgA levels than children with obesity, morbid obesity, and MetS (p < 0.05). Cardiac MyBP-C levels of children with MetS were significantly higher than of children with normal-BMI and OB children (p < 0.05). There was no significant difference in hs-cTnT, sTWEAK, TMAO and multimerin-2 between the groups (p>0.05). These results suggested that cMyBP-C and CgA molecules may be involved in the pathogenesis of obesity-related CVDs.