460) Conclusions: Children with chronic liver disease, whether in a compensated or decompensated state, had lower serum zinc levels compared with the healthy controls. As the severity of liver disease worsened, the zinc levels decreased. The study suggests that zinc supplementation should constitute part of the micronutrient intake of children with chronic liver disease. “
“Genetic factors are believed to play a role on the development of NAFLD, as even in individuals closely matched for all clinical variables, some do not develop
hepatic steatosis, many develop only simple steatosis, while others steatohep-atitis and eventually, cirrhosis. In order to assess the role of genetic factors that may be associated with NAFLD and NASH, PNPLA3 CX5461 (patatin-like phospholipase domain-containing protein 3), APOC3 (apolipoprotein C3), and PPARG (peroxisome see more pro-liferator-activated receptor-gamma) single nucleotide polymorphisms (SNPs) were analyzed. A total of 176 patients were included
in the study. Liver magnetic resonance imaging and spectroscopy (1H-MRS) and a liver biopsy (n=131) were performed to characterize liver disease. An oral glucose tolerance test was performed to determine diabetes status and insulin resistance was calculated during the fasting state (HOMA-IR and AdipoIR [fasting plasma free fatty acids × insulin]). Polymorphisms associated with increased liver fat by 1H-MRS after adjusting for age, gender, and ethnicity check details included: rs738409 (PNPLA3: +3.4% liver fat per G allele, p=0.03) and rs2281135 (PNPLA3: +3.1% liver fat per T allele, p=0.05). Moreover,
both of these SNPs were also associated with higher plasma alanine aminotransferase levels (an increase of 7±3 IU/L per risk allele for both SNPs after adjustments for age, gender and ethnicity, p=0.04). Neither PPARG nor APOC3 had any association with liver fat content by 1H-MRS. To further characterize the mechanisms by which these SNPs may affect liver fat, their relationship with different measurements of insulin resistance was assessed. None of the examined SNPs were associated with liver (HOMA-IR), or adipose tissue (AdipoIR) insulin resistance. Regarding severity of liver disease, PNPLA3 and APOC3 SNPs were not associated with the presence of NASH, worse necroinflammation, or fibrosis. However, PPARG rs17817276 was associated with the presence of NASH: patients with the GG genotype had a lower prevalence of NASH versus other variants: 50% vs. 86%, p=0.004 (OR=0.39, p=0.03) after adjusting for age, and ethnicity. Conclusions: genetic variants may hold the answer to individual variations in the severity of NAFLD and NASH. Although PNPLA3 SNPs were associated with liver fat content, no significant association was observed with insulin resistance or with severity of NASH. PPARG rs17817276 was associated with a higher prevalence of NASH, which emphasizes the important role that thiazolidinediones (i.e.