A study conducted at the Institute of Biomedicine of the University of Eastern Finland shows that a common mutation in the PNPLA3 gene, combined with overweight, results in elevated alanine aminotransferase (ALAT) values in children. The ALAT value is an indicator of liver metabolism. In adults, this gene mutation is known to promote the accumulation of fat in the liver. The results indicate that a healthy lifestyle is already important in childhood in order to prevent the accumulation of fat in the liver, and it is especially important for those carrying the risk gene. The results were published online ahead of print in Pediatric Obesity.
According to the study, the liver ALAT values of overweight children who are carriers of the gene mutation are more elevated than those of other children. The gene mutation without the presence of overweight did not elevate liver values. That is, the co-existence of extra fat tissue and the gene mutation cause the elevated liver values in childhood. Moreover, merely being overweight without being a carrier of the gene mutation is linked to elevated liver values; however, the gene mutation significantly increases the occurrence of elevated liver values.
The study included 481 healthy six-to-eight year olds from the Physical Activity and Nutrition in Children Study, an ongoing lifestyle intervention study. The significance of the research findings for public health is emphasized by the fact that 41% of the children who participated in the study were carriers of the PNPLA3 gene mutation associated with fatty liver, and 15% were overweight. Read the study abstract.
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