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RESEARCH PRODUCT

The rs11187533 C>T Variant of the <b><i>FFAR4</i></b> Gene Is Associated with Lower Levels of Fasting Glucose and Decreases in Markers of Liver Injury in Children with Obesity

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<b><i>Introduction:</i></b> Genetic factors can modulate the development of associated comorbidities in obesity. It has been shown that loss-of-function variants of the <i>free fatty acid receptor 4 (FFAR4)</i> gene negatively affect obesity comorbidities such as insulin resistance and fatty liver disease. <b><i>Objective:</i></b> To test the relationships of metabolic factors in children with obesity with variants of the <i>FFAR4</i> gene. <b><i>Methods:</i></b> We performed an association study of 3 single nucleotide polymorphisms (SNPs) of <i>FFAR4</i> (rs10882273 T>C, rs12243124 T>C, and rs11187533 C>T) covering the last intron and last exon of <i>FFAR4</i> in a cohort of 203 children with obesity. Cardiometabolic factors were determined, including parameters related to insulin resistance, liver injury, and high-sensitivity C-reactive protein as an inflammatory marker. <b><i>Results:</i></b> Significant genotype – phenotype interactions occurred between the rs11187533 SNP and glucose levels (<i>p</i> = 0.011). Moreover, we identified 2 marginally significant associations between this SNP and the hepatic enzymes alanine aminotransferase (<i>p</i> = 0.022) and gamma-glutamyltransferase (<i>p</i> = 0.015). The homozygous minor allele genotype (TT) was associated with a decrease in glucose levels. <b><i>Conclusion:</i></b> The homozygous minor allele genotype of the rs11187533 SNP might be protective against metabolic consequences accompanying obesity and could allow the identification of metabolically healthy obese individuals at early ages.