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FTO and PLAG1 Genes Expression and FTO Methylation Predict Changes in Circulating Levels of Adipokines and
Wojciech Czogała1,2, Wojciech Strojny1, Magdalena Schab1
1Department of Pediatric Oncology and Hematology, University Children's Hospital of Krakow, 30-663 Krakow, Poland.
Insights
This study links FTO and PLAG1 gene expression and methylation to adipokines and gastrointestinal hormones in children. Results show correlations between these genes and metabolic parameters, suggesting roles in adiposity.
Area of Science:
- Pediatric Endocrinology
- Molecular Biology
- Metabolic Research
Background:
- Adipokines and gastrointestinal hormones are key metabolic regulators.
- Epigenetic factors and gene expression influence hormone levels in children.
- The roles of FTO (alpha-ketoglutarate dependent dioxygenase) and PLAG1 (zinc finger) in metabolism require further elucidation.
Purpose of the Study:
- To investigate the relationship between FTO and PLAG1 gene methylation and expression levels.
- To assess the association of these gene alterations with concentrations of specific gastrointestinal hormones and adipokines in children.
- To explore the potential involvement of FTO and PLAG1 in the pathogenesis of childhood adiposity.
Main Methods:
- Cross-sectional study involving 26 children with diverse BMI.
- Gene expression and methylation analysis in peripheral blood mononuclear DNA using microarray and restriction enzyme methods.
- Quantification of peptide hormone and adipokine concentrations via enzyme immunoassay.
Main Results:
- FTO and PLAG1 gene expression significantly correlated with adipokine levels (leptin, apelin, leptin receptor).
- FTO methylation and expression showed negative correlations with resistin and visfatin.
- FTO gene correlated with cholecystokinin and fibroblast growth factor 21; PLAG1 expression linked to cholecystokinin and GLP-1.
- PLAG1 expression predicted increased leptin and decreased ghrelin.
Conclusions:
- The FTO gene is associated with concentrations of hormones from adipose tissue and the gastrointestinal tract.
- The PLAG1 gene may play a role in the development of adiposity.
- Further research is needed to clarify the precise molecular mechanisms involved.
Abstract:
Adipokines and gastrointestinal tract hormones are important metabolic parameters, and both epigenetic factors and differential gene expression patterns may be associated with the alterations in their concentrations in children. The function of the FTO gene (FTO alpha-ketoglutarate dependent dioxygenase) in the regulation of the global metabolic rate is well described, whereas the influence of protooncogene PLAG1 (PLAG1 zinc finger) is still not fully understood. A cross-sectional study on a group of 26 children with various BMI values (15.3-41.7; median 28) was carried out. The aim was to evaluate the dependencies between the level of methylation and expression of aforementioned genes with the concentration of selected gastrointestinal tract hormones and adipokines in children. Expression and methylation were measured in peripheral blood mononuclear DNA by a microarray technique and a restriction enzyme method, respectively. All peptide concentrations were determined using the enzyme immunoassay method. The expression level of both FTO and PLAG1 genes was statistically significantly related to the concentration of adipokines: negatively for apelin and leptin receptor, and positively for leptin. Furthermore, both FTO methylation and expression negatively correlated with the concentration of resistin and visfatin. Cholecystokinin was negatively correlated, whereas fibroblast growth factor 21 positively correlated with methylation and expression of the FTO gene, while FTO and PLAG1 expression was negatively associated with the level of cholecystokinin and glucagon-like peptide-1. The PLAG1 gene expression predicts an increase in leptin and decrease in ghrelin levels. Our results indicate that the FTO gene correlates with the concentration of hormones produced by the adipose tissue and gastrointestinal tract, and PLAG1 gene may be involved in adiposity pathogenesis. However, the exact molecular mechanisms still need to be clarified.
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