Inverse Association Between Serum 25-Hydroxyvitamin D and Nonalcoholic Fatty Liver Disease
Yuan S, Larsson SC
Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association · 32 citations
How it was studied
- Design
- Meta-analysis (indexed by PubMed)
- Studied in
- People
- Main outcome
- Clinical events such as disease or death
Who paid for it
- Funding
- Independent funding
- Government
- Vetenskapsrådet
- Government
- Forskningsrådet om Hälsa, Arbetsliv och Välfärd
- Grants
- Forskningsrådet om Hälsa, Arbetsliv och Välfärd (2019‐00977); Vetenskapsrådet (2019-00977); Vetenskapsrådet (2018-00123); Forskningsrådet om Hälsa, Arbetsliv och Välfärd (2018-00123); Vetenskapsrådet (2018-)
Based on 2 listed funder(s).
Publication
- Published
- 2022-01-31 · Clin Gastroenterol Hepatol · vol. 21 · issue 2 · pp. 398–405.e4
- Publisher
- Elsevier BV
- Cited
- 42 citations · more than 97% of similar papers · 5.1× the field average
- Impact
- Top 10% most cited in its field
- References
- 46 works
- Access
- Open access (hybrid journal) · CC-BY
- Research areas
- Vitamin D Research Studies · Liver Disease Diagnosis and Treatment · Growth Hormone and Insulin-like Growth Factors
- Keywords
- Nonalcoholic fatty liver disease, Mendelian randomization, Medicine, Odds ratio, Internal medicine, Genome-wide association study, Vitamin D and neurology, Confounding, Gastroenterology, Confidence interval, vitamin D deficiency, Genetic association, Fatty liver, Disease, Single-nucleotide polymorphism, Genetics, Genotype, Gene, Biology, Genetic variants
- MeSH
- humans, vitamin d, risk factors, polymorphism, single nucleotide, genome-wide association study, mendelian randomization analysis, non-alcoholic fatty liver disease
2 authors
From SE
- Shuai YuanKarolinska Institutet
- Susanna C. LarssonUppsala University; Karolinska Institutet
Abstract
Background & aims
Serum 25-hydroxyvitamin D [S-25(OH)D] and nonalcoholic fatty liver disease (NAFLD) are correlated in many observational studies, whereas the causality of this association is uncertain, especially in European populations. We conducted a bidirectional Mendelian randomization study to determine the association between S-25(OH)D and NAFLD.
Methods
Seven and 6 independent genetic variants associated with S-25(OH)D and NAFLD at the genome-wide-significance level, respectively, were selected as instrumental variables. Summary-level data for S-25(OH)D were obtained from the Study of Underlying Genetic Determinants of Vitamin D and Highly Related Traits consortium including 79,366 individuals. Summary-level data for NAFLD were available from a genome-wide association meta-analysis (1483 cases and 17,781 controls), the FinnGen consortium (894 cases and 217,898 controls), and the UK Biobank study (275 cases and 360,919 controls). Summary-level data for 4 liver enzymes were obtained from the UK Biobank.
Results
There were genetic correlations of S-25(OH)D with NAFLD and certain liver enzymes. Genetically predicted higher levels of S-25(OH)D were consistently associated with a decreased risk of NAFLD in the 3 sources. For a 1-SD increase in genetically predicted S-25(OH)D levels, the combined odds ratio of NAFLD was 0.78 (95% confidence interval [CI], 0.69 to 0.89). Genetically predicted higher levels of S-25(OH)D showed a borderline association with aspartate aminotransferase levels (change -1.17; 95% CI, -1.36 to 0.01). Genetic predisposition to NAFLD was not associated with S-25(OH)D (change 0.13; 95% CI, -1.26 to 0.53).
Conclusions
Our findings have clinical implications as they suggest that increased vitamin D levels may play a role in NAFLD prevention in European populations.
Abstract via Europe PMC. Copyright remains with the authors or publisher (CC BY).
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