Prospective Analysis of Small Metabolites and Obesity-Related Liver Disease in Hepatitis B
Date Issued
2014
Date
2014
Author(s)
Hsu, Chi-Jen
Abstract
Background: Nonalcoholic fatty liver disease (NAFLD) occurs due to excessive fat accumulation in the liver cells, which is becoming an increasingly common cause of hepatic disease. Obesity and related metabolic syndrome increase the risk of NAFLD. The purpose of this study was to understand the mechanisms underlying the relationship between abnormal metabolism and obesity-related liver diseases in hepatitis B, with the use of metabolomics approach.
Materials and methods: Study subjects included a total of 711 overweight or obese men with hepatitis B, who were recruited from a cohort study of civil servants. Information on demographics, lifestyle habits, and medical history was obtained from a structured questionnaire. Metabolomics profiles of baseline serum samples were deter-mined using 1H nuclear magnetic resonance (NMR)-based metabolomics assay. Partial least squares discriminant analysis (PLS-DA) was applied to analyze the profiling data to identify the distinguishing metabolites of dyslipidemia and liver biochemical and ultrasonographic abnormalities as well as hepatocellular carcinoma.
Results: A total of 22 metabolites was identified, 12 of which were important for classification of triglycerides (TG) abnormality, including 4 that were up-regulated and 8 that were down-regulated in participants with TG abnormality. The up-regulation of 4 metabolites, including acetone, VLDL/LDL (CH3-(CH2)n), VLDL/LDL (CH3-(CH2)n) and unsaturated lipid, tend to be positively associated with fatty liver but were significantly, inversely associated with liver cirrhosis. The down-regulation of 8 metabolites, including citrate, creatine, beta-glucose, glutamine, methanol, proline, tyrosine and valine, tend to be inversely associated with fatty liver but significantly, positively associated with liver cirrhosis. On the other hand, none of these 12 metabolites were significantly associated with hepatocellular carcinoma.
Conclusion: Our preliminary results showed an association between elevated TG and an altered metabolite signature. The altered metabolites in relation to TG abnormality revealed no consistent patterns in any type of liver abnormalities.
Subjects
肥胖
非酒精性脂肪肝病
代謝質體學
SDGs
Type
thesis
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