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The rs72613567:TA Variant in theHydroxysteroid 17-beta Dehydrogenase 13Gene Reduces Liver Damage in Obese Children

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LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/MPG.0000000000002573

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beta dehydrogenase; children; damage; liver; obese; steatosis

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We first investigated in obese children the protective role of thehydroxysteroid 17-beta dehydrogenase 13(HSD17B13)rs72613567:TA variant in liver damage. Six hundred eighty-five obese children were genotyped forHSD17B13,patatin-like phospholipase domain containing 3(PNPLA3),transmembrane 6 superfamily member 2(TM6SF2), andmembrane bound O-acyltransferase domain containing 7(MBOAT7) polymorphisms and underwent anthropometrical, ultrasonographic, and biochemical evaluation. Indirect measurement of liver fibrosis (Pediatric NAFLD Fibrosis Index [PNFI]) was calculated. The population was clustered in 2 genetic risk groups based on the numbers of steatogenic alleles (low: carriers up to 3 risk alleles, high: 4-6 risk alleles). Carriers of theHSD17B13rare A allele showed lower percentage of hepatic steatosis and both lower serum transaminase and PNFI levels than noncarriers, even after adjustments for confounders. These findings were also confirmed in both risk groups. We demonstrated the protective effect of the rs72613567:TA HSD17B13 variant in reducing liver damage in obese children regardless of genetic predisposition.

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