Gene responsible for fatty liver disease in obese kids identified
Last Updated: Friday, April 20, 2012, 11:56
  

Washington: Researchers have found that obese youths with particular genetic variants may be more prone to fatty liver disease, a leading cause of chronic liver disease in children and adolescents in industrialized countries.



Led by Nicola Santoro, M.D., associate research scientist in the Department of Pediatrics at Yale School of Medicine, the researchers measured the hepatic, or liver, fat content of children using magnetic resonance imaging.

The study focused on three ethnic groups and included 181 Caucasian, 139 African-American and 135 Hispanic children who were, on average, age 13.

“We observed that a common genetic variant known as Patatin-like phospholipase domain containing protein-3 (PNPLA3) working with a regulatory protein called glucokinase (GCKR), was associated with increased triglycerides, very low-density lipoproteins levels, and fatty liver,” said Santoro.

Santoro explained that his observations could help unravel the genetic mechanisms that contribute to liver fat metabolism.

“This may drive the decisions about future drug targets to treat hypertriglyceridemia and non-alcoholic fatty liver disease,” he said.

Childhood obesity is a global health concern. Experts say nonalcoholic fatty liver disease is now the leading cause of chronic liver disease in children and adolescents in industrialized countries.

“Our findings confirm that obese youths with genetic variants in the GCKR and PNPLA3 genes may be more susceptible to fatty liver disease,” said Santoro, who is cautious about automatically extending this observation to the overall population.

“Our data refer to a population of obese children and adolescents. I think that further studies in a larger sample size involving lean subjects and adults may help to further define in more details these associations,” he concluded.

The study has been published in the March issue of the journal Hepatology.

ANI


First Published: Friday, April 20, 2012, 11:56



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