期刊
ALIMENTARY PHARMACOLOGY & THERAPEUTICS
卷 56, 期 2, 页码 321-329出版社
WILEY
DOI: 10.1111/apt.16948
关键词
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资金
- National Institutes of Health (NIH) [P30CA006973-52S3]
- NIH Intramural Research Program
This study identified a relationship between bile acid levels and non-alcoholic fatty liver disease (NAFLD) at the population level. Individuals with NAFLD had significantly higher levels of certain bile acids, indicating hepatic overproduction of bile acids may be involved in the pathogenesis of NAFLD.
Background Non-alcoholic fatty liver disease (NAFLD) has emerged as a major liver disease worldwide. Bile acid dysregulation has been suggested to be a key feature in its pathogenesis and progression. Aims To characterise the relationship between bile acid levels and NAFLD on the population level. Methods A cross-sectional study in Guatemala was conducted in 2016 to examine the prevalence of NAFLD. Participants (n = 415) completed questionnaires, donated blood samples and had a brief medical exam. NAFLD was determined by calculation of the fatty liver index. The levels of 15 circulating bile acids were determined by LC-MS/MS. Adjusted prevalence odds ratios (PORadj) and 95%CI were calculated to examine the relationships between bile acid levels (in tertiles) and NAFLD. Results Persons with NAFLD had significantly higher levels of the conjugated primary bile acids glycocholic acid (GCA) (PORadj T3 vs T1 = 1.85), taurocholic acid (TCA) (PORadj T3 vs T1 = 2.45) and taurochenodeoxycholic acid (TCDCA) (PORadj T3 vs T1 = 2.10), as well as significantly higher levels the unconjugated secondary bile acid, deoxycholic acid (DCA) (PORadj T3 vs T1 = 1.78) and its conjugated form, taurodeoxycholic acid (TDCA) (PORadj T3 vs T1 = 1.81). Conclusions The bile acid levels of persons with, and without, NAFLD differed significantly. Among persons with NAFLD, higher levels of the conjugated forms of CA (i.e. GCA, TCA) and the secondary bile acids that derive from CA (i.e. DCA, TDCA) may indicate there is hepatic overproduction of CA, which may affect the liver via aberrant signalling mediated by the bile acids.
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