Correlation Of Nonalcoholic Fatty Liver Disease Research Articles

System biology analysis reveals the role of voltage-dependent anion channel in mitochondrial dysfunction during non-alcoholic fatty liver disease progression into hepatocellular carcinoma.

Non‐alcoholic fatty liver disease (NAFLD) is one of the most common causes of hepatocellular carcinoma (HCC), but the underlying mechanisms behind the correlation of NAFLD with HCC are unclear. We aimed to uncover the genes and potential mechanisms that drive this progression. This study uncovered the genes and potential mechanisms through a multiple ’omics integration approach. Quantitative proteomics combined with phenotype‐association analysis was performed. To investigate the potential mechanisms, a comprehensive transcriptome/lipidome/phenome‐wide association analysis was performed in genetic reference panel BXD mice strains. The quantitative proteomics combined with phenotype‐association results showed that VDAC1 was significantly increased in tumor tissues and correlated with NAFLD‐related traits. Gene co‐expression network analysis indicated that VDAC1 is involved in mitochondria dysfunction in the tumorigenic/tumor progression. The association between VDAC1 and mitochondria dysfunction can be explained by the fact that VDAC1 was associated with mitochondria membrane lipids cardiolipin (CL) composition shift. VDAC1 was correlated with the suppression of mature specie CL(LLLL) and elevation level of nascent CL species. Such profiling shift was supported by the significant positive correlation between VDAC1 and PTPMT1, as well as negative correlation with CL remodeling enzyme Tafazzin (TAZ). This study confirmed that the expression of VADC1 was dysregulated in NAFLD‐driven HCC and associated with NAFLD progression. The VDAC1‐driven mitochondria dysfunction is associated with cardiolipin composition shift, which causes alteration of mitochondria membrane properties.

PREVALENCE OF FATTY LIVER CHANGES ON NON-CONTRAST ENHANCED COMPUTED TOMOGRAPHY AND ITS ASSOCIATED RISK FACTORS

Background: The Fourth National Health and Morbidity Survey completed in 2011, revealed that 27.2% of Malaysian adults aged 18 years and above are obese, while 33.3% are pre-obese, with increasing prevalence of obese children. Together with observation of “ethnic lipodystrophy” in South Asians population and increasing prevalence of non-alcoholic fatty liver disease (NAFLD) in Asian population, further study of NAFLD in Malaysian population with their associated risk factors is necessary. Materials and Methods: A prospective cross-sectional study of patients who underwent CT Urography (CTU) examination, selected through simple random sampling. Presence of NAFLD was determined based on liver CT value of <40 HU and CT Liver-Spleen attenuation ratio. Association and correlation of NAFLD with Body Mass Index (BMI), abdominal wall subcutaneous fat thickness and biochemical markers were calculated. Result: Forty-six percent (46%) of study population had NAFLD, with male predominance. There were significant association of NAFLD with BMI, abdominal wall subcutaneous fat thickness and lower serum HDL level. Conclusion: Increasing prevalence of NAFLD with increasing BMI, thicker abdominal wall subcutaneous fat thickness and decreasing serum HDL level Keywords: non-alcoholic fatty liver disease, risk factors, non-contrast enhanced CT, subcutaneous wall thickness

Correlates and Heritability of Nonalcoholic Fatty Liver Disease in a Minority Cohort

Nonalcoholic fatty liver disease (NAFLD) is associated with obesity and insulin resistance. The condition disproportionately affects Hispanic Americans. The aims of this study were to examine the risk factors and heritability of NAFLD in 795 Hispanic American and 347 African-American adults participating in the Insulin Resistance Atherosclerosis Study (IRAS) Family Study. Computed tomography (CT) scans of the abdomen were evaluated centrally for measures of liver-spleen (LS) density ratio and abdominal fat distribution. Other measures included insulin sensitivity (SI) calculated from a frequently sampled intravenous glucose tolerance test and various laboratory measures. Statistical models which adjust for familial relationships were estimated separately for the two ethnic groups. Heritability was calculated using a variance components approach. The mean age of the cohort was 49 years (range 22-84); 66% were female. NAFLD (LS ratio<1) was more common in Hispanic Americans (24%) than African Americans (10%). NAFLD was independently associated with SI and visceral adipose tissue (VAT) area in both ethnic groups, although the proportion of explained variance was considerably higher in the Hispanic models. Adiponectin contributed significantly in the African-American models whereas triglycerides (TGs) and plasminogen activator inhibitor 1 (PAI-1) contributed only in the Hispanic models. Liver density was modestly heritable in both ethnic groups (h2 approximately 0.35). In summary, the prevalence of NAFLD was twofold greater in Hispanic than African Americans. Certain correlates of NAFLD were similar between the ethnic groups, whereas others were distinct. NAFLD was modestly heritable. These findings suggest that NAFLD may have a differing environmental and/or genetic basis in these ethnic groups.