Characterization of European ancestry nonalcoholic fatty liver disease-associated variants in individuals of African and Hispanic descent

Hepatology. 2013 Sep;58(3):966-75. doi: 10.1002/hep.26440. Epub 2013 Jul 16.

Abstract

Nonalcoholic fatty liver disease (NAFLD) is an obesity-related condition affecting over 50% of individuals in some populations and is expected to become the number one cause of liver disease worldwide by 2020. Common, robustly associated genetic variants in/near five genes were identified for hepatic steatosis, a quantifiable component of NAFLD, in European ancestry individuals. Here we tested whether these variants were associated with hepatic steatosis in African- and/or Hispanic-Americans and fine-mapped the observed association signals. We measured hepatic steatosis using computed tomography in five African American (n = 3,124) and one Hispanic American (n = 849) cohorts. All analyses controlled for variation in age, age(2) , gender, alcoholic drinks, and population substructure. Heritability of hepatic steatosis was estimated in three cohorts. Variants in/near PNPLA3, NCAN, LYPLAL1, GCKR, and PPP1R3B were tested for association with hepatic steatosis using a regression framework in each cohort and meta-analyzed. Fine-mapping across African American cohorts was conducted using meta-analysis. African- and Hispanic-American cohorts were 33.9/37.5% male, with average age of 58.6/42.6 years and body mass index of 31.8/28.9 kg/m(2) , respectively. Hepatic steatosis was 0.20-0.34 heritable in African- and Hispanic-American families (P < 0.02 in each cohort). Variants in or near PNPLA3, NCAN, GCKR, PPP1R3B in African Americans and PNPLA3 and PPP1R3B in Hispanic Americans were significantly associated with hepatic steatosis; however, allele frequency and effect size varied across ancestries. Fine-mapping in African Americans highlighted missense variants at PNPLA3 and GCKR and redefined the association region at LYPLAL1.

Conclusion: Multiple genetic variants are associated with hepatic steatosis across ancestries. This explains a substantial proportion of the genetic predisposition in African- and Hispanic-Americans. Missense variants in PNPLA3 and GCKR are likely functional across multiple ancestries.

Publication types

  • Comparative Study
  • Meta-Analysis

MeSH terms

  • Adaptor Proteins, Signal Transducing / genetics
  • Adult
  • Aged
  • Black People / ethnology
  • Black People / genetics*
  • Black or African American
  • Chondroitin Sulfate Proteoglycans / genetics
  • Cohort Studies
  • Fatty Liver / ethnology
  • Fatty Liver / genetics*
  • Female
  • Gene Frequency / genetics
  • Genetic Predisposition to Disease / ethnology
  • Genetic Predisposition to Disease / genetics*
  • Genetic Variation / genetics*
  • Hispanic or Latino / ethnology
  • Hispanic or Latino / genetics*
  • Humans
  • Lectins, C-Type / genetics
  • Lipase / genetics
  • Lysophospholipase / genetics
  • Male
  • Membrane Proteins / genetics
  • Middle Aged
  • Nerve Tissue Proteins / genetics
  • Neurocan
  • Non-alcoholic Fatty Liver Disease
  • Phosphoprotein Phosphatases / genetics
  • White People / ethnology
  • White People / genetics*

Substances

  • Adaptor Proteins, Signal Transducing
  • Chondroitin Sulfate Proteoglycans
  • GCKR protein, human
  • Lectins, C-Type
  • Membrane Proteins
  • Nerve Tissue Proteins
  • Neurocan
  • NCAN protein, human
  • Lipase
  • adiponutrin, human
  • Lysophospholipase
  • LYPLAL1 protein, human
  • PPP1R3A protein, human
  • Phosphoprotein Phosphatases