Lower adropin expression is associated with oxidative stress and severity of nonalcoholic fatty liver disease
Abstract
Background & aims Adropin has been reported to be involved in metabolic disorders, including nonalcoholic fatty liver disease (NAFLD). However, the clinical relevance of adropin expression to the histological severity of NAFLD is unclear. This study aimed to investigate adropin expression in biopsy-proven NAFLD patients.Methods This case-control study enrolled a total of 109 participants, including 15 normal histological controls, 26 nonalcoholic fatty liver (NAFL), 21 nonalcoholic steatohepatitis (NASH) subjects and B-ultrasound NAFLD-free normal controls matched to the cases based on age and sex (the case:control ratio was 1:1). Liver biopsies were obtained and histological characteristics were assessed. Primary murine hepatocytes were isolated from C57BL/6J mice and incubated with doses of palmitate to induce oxidative stress.Results The serum adropin level in NASH patients was 9.99 ± 5.51 ng/ml, significantly lower than that in B-ultrasound normal controls (22.70 ± 6.32 ng/ml), histological normal controls (21.93 ± 6.63 ng/ml) and NAFL patients (17.82 ± 6.90 ng/ml). Serum adropin levels were negatively correlated with the histological severity of NAFLD. The lower serum adropin level predicted NASH (area under the ROC curve: 87.1%). Adropin expression in serum and liver was also negatively associated with hepatic MDA and serum 8-iso-PGF2α levels. Furthermore, palmitate rather than oleate induced oxidative stress in a dose-dependent manner with a gradient decrease in adropin expression in primary murine hepatocytes. Adropin overexpression or treatment ameliorated palmitate-induced oxidative stress in hepatocytes.Conclusions Circulating adropin was inversely associated with the oxidative stress and histological severity of NAFLD. It may play an important role in the development of NAFLD.
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Lower adropin expression may play an important role in the progression of NAFLD to severe NASH.
“It is also negatively related to the pathological changes in NAFLD, suggesting that the lower adropin expression may play an important role in the progression of NAFLD to severe NASH.”
From Adipokines, Myokines, and Hepatokines: Crosstalk and Metabolic Repercussions (2021) · cites this paper as [113]
Adropin is negatively related to the pathological changes in NAFLD.
“It is also negatively related to the pathological changes in NAFLD, suggesting that the lower adropin expression may play an important role in the progression of NAFLD to severe NASH.”
From Adipokines, Myokines, and Hepatokines: Crosstalk and Metabolic Repercussions (2021) · cites this paper as [113]
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- Authors
- Chen, X., Sun, X., Shen, T., Chen, Q., Chen, S., Pang, J., Mi, J., Tang, Y., You, Y., Xu, H., & Ling, W.
- Affiliations
- Sun Yat-sen University (CN)
- Guangdong Pharmaceutical University (CN)
- Corresponding author
- Ling, Wenhua
- Venue
- Free Radical Biology and Medicine
- Publisher
- Elsevier BV
- Published
- 2020-11
- Volume
- 160
- Pages
- 191-198
- ISSN
- 0891-5849 (ISSN-L)
- OpenAlex
- W3049733492
- Cited by
- 30
- References
- 34
- Citations by year
- 2026: 2 · 2025: 7 · 2024: 5 · 2023: 5 · 2022: 7 · 2021: 4
- FWCI
- 2.87
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Free Radical Biology and Medicine (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China
- Guangzhou Research Collaborative Innovation Projects
- Topics
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Keywords
- adropin, non-alcoholic fatty liver disease, nonalcoholic steatohepatitis, oxidative stress, histological severity, malondialdehyde, 8-isoprostane, palmitate, hepatocytes, biomarkers, liver biopsy
- MeSH terms
- Animals, Humans, Liver, Mice, Inbred C57BL, Biomarkers, Case-Control Studies, Oxidative Stress, Intercellular Signaling Peptides and Proteins, Mice, Non-alcoholic Fatty Liver Disease
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