Abstract
Genome-wide association studies have identified single-nucleotide polymorphisms (SNPs) that increase the risk of developing non-alcoholic fatty liver disease (NAFLD). One purpose of this study was to determine the frequencies of NAFLD susceptibility SNPs in a non-Hispanic white and Hispanic population who attended a clinic in northeast Albuquerque, NM. Another goal was to determine associations with selected indicators in this New Mexican population. This cohort study involving 168 volunteer subjects in the NM population (88 non-Hispanic whites, 63 Hispanics, 4 Native Americans, 11 Asian Americans, 2 unreported ethnicity). Eight SNPs within 6 NAFLD susceptibility genes including PNPLA3 (rs738409), LYPLAL1 (rs12137855), APOC3 (rs2854116, rs2854117), GCKR (rs780094, rs741038), FABP2 (rs1799883), PEMT (rs7946) were analyzed by genotyping using the TaqMan genotyping assay (Applied Biosystems, Foster City, CA). Statistical analyses were carried out using statistical package SAS 9.3. The NAFLD allele frequencies were similar in non-Hispanic whites and Hispanics except for PNPLA3 (rs738409), FABP2 (rs1799883), and PEMT (rs7946). Eight SNPs in 5 NAFLD susceptibility genes were significantly associated OR marginally associated with selected indicators for NAFLD, metabolic syndrome, overweight, obesity, insulin resistance, type 2 diabetes, hypertension, dyslipidemia. No SNPs were significantly associated with the same indicator in both the non-Hispanic white and Hispanic groups. In this population of non-Hispanic whites and Hispanics, there were only heterozygotes for the APOC3 derived alle le whereas for all other genes tested, both heterozygotes and homozygotes were found. Associations of alleles with indicators of chronic disease were different in non-Hispanic whites compared to Hispanics.
Highlights
Non-alcoholic fatty liver disease (NAFLD) is defined as the presence of fat deposits in > 5% of hepatocytes as diagnosed by a liver biopsy or magnetic resonance imaging without an association to alcohol intake or medication[1]
The percentages of NAFLD allele frequencies in this cohort were similar in non-Hispanic whites and Hispanics except forPNPLA3, FABP2, and PEMT and for each of these genes the major allele was more frequent for non-Hispanic whites whereas in Hispanics the major and minor alleles had similar frequencies
The derived allele was the major allele of PNPLA3, Glucokinase Regulatory Protein (GCKR), and PEMT and the minor allele of APOC3, GCKR, FABP2, and LYPLAL1 for non-Hispanic whites and Hispanics alike
Summary
Non-alcoholic fatty liver disease (NAFLD) is defined as the presence of fat deposits in > 5% of hepatocytes as diagnosed by a liver biopsy or magnetic resonance imaging without an association to alcohol intake or medication[1]. NAFLD affects 20-30% of the adult population in the United States[2]. The major risk factors for NAFLD include overweight, obesity, insulin resistance, type 2 diabetes, hyper-. Received date: June 26, 2015 Accepted date: July 21, 2015 Published date: July 27, 2015. Evidence suggests that NAFLD precedes the development of type 2 diabetes[6,7]. When individuals had both type 2 diabetes and obesity, advanced fibrosis was evident in 66% of patients with NAFLD[4]
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