The number of studies examining the relationship between obesity and fetuin-A in children is limited [14–18, 21]. In adult studies; a relationship between fetuin-A levels and obesity, insulin resistance, fatty liver has been shown and increased cardiovascular risk associated with fetuin-A has been emphasized [6, 11–13]. In our study, similar to the study of Pampanini et al., no difference was found in terms of fetuin-A levels in the obese and control groups [14]. Although there are studies revealing higher fetuin-A levels in obese children, there are studies in the literature with conflicting results. In another study evaluating 45 obese and 30 non-obese children, fetuin-A level was found to be higher in obese patients [15]. However, no relationship was found between fetuin-A and other parameters (glucose, insulin, HOMA-IR, lipid parameters, ALT, GGT) examined in this study. In a study comparing obese and normal weight patients, the relationship between glucose, insulin, lipid parameters, blood pressure, subcutaneous and cardiac fat accumulation and fetuin-A level was evaluated. Fetuin-A level was found to be significantly higher in the obese group. In addition, a correlation was found between fetuin-A level and insulin, HOMA-IR, subcutaneous and subepicardial fat accumulation in both groups [16]. In another study investigating cardiovascular disease risk in obese children, no difference was found in terms of fetuin-A, when obese children / adolescents with and without metabolic syndrome were compared [17].
Although 33 of the subjects in our study had fatty liver, no significant difference was found between the groups with and without fatty liver in terms of fetuin-A levels. Only two of the patients had elevated liver function tests and the diagnosis of fatty liver was made ultrasonographically. In a large cohort study of children comparing 160 obese and 23 non-obese children [14], higher fetuin-A levels were detected in obese patients with fatty liver on ultrasound, than those without. However, no difference was found in terms of fetuin-A level between obese patients diagnosed with non-alcoholic steatohepatitis (NASH) by liver biopsy and those who were diagnosed with simple steatosis (nonNASH) by biopsy. In this study, it was stated that unlike adults, the severity of liver damage and fetuin-A level were not correlated in children. In addition, no difference was found between fetuin-A levels of non-obese patients and those diagnosed with NAFLD by ultrasonography or biopsy. In some adult studies comparing fetuin-A levels in obese patients with and without fatty liver, no difference was found [12].
In a longitudinally designed study in which 36 obese and 14 normal-weight children were compared, there was no difference in terms of fetuin-A between both groups, while fetuin-A levels were found to be significantly higher in 12 obese children with fatty liver [18]. There was no difference in terms of fetuin-A between obese cases without fatty liver and normal weight cases. In this study, it was emphasized that especially fatty liver leads to an increase in the level of fetuin-A. In another study conducted with obese children, intra-group comparisons was made and fetuin-A levels were found to be higher in those with fatty liver [15]. In an adult study comparing obese and non-obese patients with type 2 DM and normal weight patients with type 2 DM and patients with normal glucose tolerance (NGT), fetuin-A was found to be highest in obese patients with type 2 DM [6]. In obese and NGT individuals, fetuin-A levels were found higher than non-obese individuals. In our study, since there was one case with Type 2 DM and four cases with impaired glucose tolerance, statistical analysis could not be made in this respect.
In a study evaluating the fetuin-A level in patients with type 1 DM, when obese cases were evaluated separately, a positive correlation was found between daily insulin dose and fetuin-A (fetuin-A levels were found to be higher in patients with insulin dose > 1 / kg / day) [10]. In the same study, no relationship was found between lipid parameters and blood pressure and fetuin-A. In addition, it was found that fetuin-A levels were lower in both normal / underweight and overweight / obese type 1 DM patients compared to obese type 2 DM patients.
In our study, no relationship was found between lipid parameters and fetuin-A. Although there are studies in the literature that showed a relationship between low HDL as a metabolic syndrome component and fetuin-A level [21], there are also studies that have not found a relationship similar to our study [10, 15].
Although the factors affecting fetuin-A are not known exactly; it has been suggested that it is affected by diet, physical activity, genetic factors, acute infections and drug use [5]. In addition, although there are studies stating that it differs with age, there are also controversial studies [5, 14, 22, 23]. Among the possible reasons for the different results in the literature on fetuin-A, it has been emphasized that previous studies have a wide age range, lack of healthy control, use of different measurement methods (because the degree of post-translational modification of fetuin-A may affect the measurement accuracy) [5].