Cited by 92Liver Disease Diagnosis and TreatmentLiver physiology and pathologyAlcohol Consumption and Health Effects

The role of hepassocin in the development of non-alcoholic fatty liver disease

Wu, Hung-Tsung, Lu, Feng-Hwa, Ou, Horng-Yih, Su, Yu-Chu, Hung, Hao-Chang, Wu, Jin-Shang, Yang, Yi-Ching, Wu, Chao-Liang +1 more·2013·Journal of Hepatology

Abstract

Background & aims While non-alcoholic fatty liver disease (NAFLD) is the most common risk factor of chronic liver disease, the mechanisms that initiate its development are obscure. Hepassocin (HPS) is a hepatokine that has been reported to be involved in liver regeneration. In addition to the mitogenic activity of HPS, HPS expression is decreased in patients with hepatoma. However, the role of HPS in NAFLD is still unknown.Methods A total of 393 subjects with (n=194) or without (n=199) NAFLD were enrolled to evaluate the serum HPS concentration. In order to clarify the causal inference between HPS and NAFLD, we used experimental animal and cell models. Hepatic overexpression or silencing of HPS was achieved by lentiviral vector delivery in mice and lipofectamine transfection in HepG2 cells. Lipogenesis related proteins were detected by Western blots. The expression of inflammatory factors was determined by real-time polymerase chain reaction.Results Subjects with NAFLD had a higher serum HPS concentration than those without it. Overexpression of HPS increased hepatic lipid accumulation and NAFLD activity scores (NAS), whereas deletion of HPS improved high fat diet-induced hepatic steatosis and decreased NAS in mice. Additionally, oleic acid, a steatogenic reagent, increased HPS expression in hepatocytes. Furthermore, overexpression of HPS in HepG2 cells induced lipid accumulation through an extracellular signal-regulated kinase 1/2 (ERK1/2)-dependent pathway, whereas deletion of HPS decreased oleic acid-induced lipid accumulation.Conclusions The present study provides evidence that HPS plays an important role in NAFLD and induces hepatic lipid accumulation through an ERK1/2-dependent pathway.

Integrity signals

Registry

Crossref · 10.1016/j.jhep.2013.06.004

Cites

28 of 28 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Hepatic expression of hepassocin increases in mice with high-fat diet-induced NAFLD.

    “Several studies demonstrated that hepatic expression of hepassocin increased in mice with high-fat diet-induced NAFLD [217,220,221].”

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Wu, H.-T., Lu, F.-H., Ou, H.-Y., Su, Y.-C., Hung, H.-C., Wu, J.-S., Yang, Y.-C., Wu, C.-L., & Chang, C.-J.
Affiliations
  • National Cheng Kung University Hospital (TW)
  • National Cheng Kung University (TW)
Corresponding author
Chang, Chih-Jen
Venue
Journal of Hepatology
Publisher
Elsevier BV
Published
2013-11
Volume
59
Issue
5
Pages
1065-1072
ISSN
0168-8278 (ISSN-L)
OpenAlex
W2067797550
Cited by
92
References
28
Citations by year
2026: 7 · 2025: 7 · 2024: 8 · 2023: 8 · 2022: 17 · 2021: 8 · 2020: 9 · 2019: 15 · 2018: 3 · 2017: 4 · 2016: 1 · 2015: 3 · 2014: 2
FWCI
1.46
Type
journal article
Language
en
Update notices
erratum (2017-02-01)
Open access
closed
Locations
  • Journal of Hepatology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
  • Health Sciences › Medicine › Hepatology › Liver physiology and pathology
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Alcohol Consumption and Health Effects
Keywords
non-alcoholic fatty liver disease, hepatokines, hepatic steatosis, hepatic lipid accumulation, ERK signaling, oleic acid, high-fat diet, serum biomarkers, liver regeneration, inflammation
MeSH terms
Aged, Animals, Cells, Cultured, Disease Models, Animal, Fatty Liver, Female, Fibrinogen, Humans, Male, Mice, Inbred C57BL, Middle Aged, Neoplasm Proteins, Case-Control Studies, Gene Deletion, Oleic Acid, MAP Kinase Signaling System, Hepatocytes, Lipid Metabolism, Mice, Hep G2 Cells, Diet, High-Fat, Non-alcoholic Fatty Liver Disease

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review