High Glucose Induces Transactivation of the .ALPHA.2-HS Glycoprotein Gene Through the ERK1/2 Signaling Pathway
Open accessAbstract
AIM: Alpha2-Heremans Schmid glycoprotein (AHSG), also known as fetuin-A, is secreted from the liver and inhibits tyrosine kinase activity of the insulin receptor. Hyperglycemia in type 2 diabetes is not only a secondary manifestation of insulin resistance, but could also be responsible for directly inducing insulin resistance in target tissues. In this study, we examined the effect of high glucose (HG) on AHSG gene transcription in the human hepatoma cell line HepG2. METHODS: AHSG transcriptional activity and protein expression were evaluated using reporter gene assays and Western blot analysis, respectively. RESULTS: D-glucose, but not L-glucose or mannitol, dose-dependently enhanced AHSG promoter activity. HG (25 mM) also increased AHSG protein expression. No protein kinase C inhibitors (bisindolylmaleimide, Ro-31-8220), an inhibitor of hexosamine biosynthesis pathway (6-diazo-5-oxo-L-norleucine), or a superoxide radical scavenger (tempol) affected HG-induced transactivation. MAPK/ERK kinase inhibitors (PD98059, U0126), but not the JNK inhibitor (SP600125) or p38 inhibitor (SB203580), significantly inhibited promoter activation by HG. CONCLUSION: Our data suggest that HG enhances AHSG transcription through activation of the ERK1/2 signaling pathway. Increased AHSG expression in the liver may be a cause of glucose toxicity in the diabetic state.
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The lack of exercise-induced decrease of fetuin A might be explained by its upregulation in the context of insulin resistance.
“The opposite may occur for fetuin A, whose lack of exercise-induced decrease might be explained by its upregulation in the context of insulin resistance [144,145].”
From The Role of Exercise in the Interplay between Myokines, Hepatokines, Osteokines, Adipokines, and Modulation of Inflammation for Energy Substrate Redistribution and Fat Mass Loss: A Review (2020) · cites this paper as [144]
The Results and Conclusion (Abstract; page unavailable) report that high glucose increased fetuin-A (AHSG) expression in HepG2 cells, providing a possible mechanism in a condition associated with insulin resistance. The paper does not study exercise or show that insulin resistance prevents an exercise-induced decrease in fetuin-A. Its Discussion (page unavailable) also says whether serum AHSG is increased in diabetic patients remains unclear. (LLM, conf=0.85)
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Willis, S. (2020) · Figshare · doi:10.26174/thesis.lboro.13214129 · Cited by 1 · see citing works
The impact of the extracellular matrix and type 1 diabetes on cardiac fibroblast activation
Shamhart, P. E. (2010) · OhioLink ETD Center (Ohio Library and Information Network)
- Authors
- Takata, H., Ikeda, Y., Suehiro, T., Ishibashi, A., Inoue, M., Kumon, Y., & Terada, Y.
- Affiliations
- University of Kochi (JP)
- Kōchi University (JP)
- Venue
- Journal of Atherosclerosis and Thrombosis
- Publisher
- Japan Atherosclerosis Society
- Published
- 2009
- Volume
- 16
- Issue
- 4
- Pages
- 448-456
- ISSN
- 1340-3478 (ISSN-L)
- 1880-3873
- OpenAlex
- W1971619045
- Cited by
- 66
- References
- 28
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 6 · 2023: 7 · 2022: 4 · 2021: 2 · 2020: 3 · 2019: 4 · 2018: 3 · 2017: 6 · 2016: 4 · 2015: 1 · 2014: 6 · 2013: 5 · 2012: 6
- FWCI
- 2.69
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by-nc-sa
- Locations
- Journal of Atherosclerosis and Thrombosis (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- fetuin-A, high glucose, ERK signaling, gene transcription, insulin resistance, type 2 diabetes, glucotoxicity, MAPK/ERK kinase, hepatocytes
- MeSH terms
- Blood Proteins, Dose-Response Relationship, Drug, Glucose, Humans, Hyperglycemia, Liver, Promoter Regions, Genetic, Signal Transduction, Transcriptional Activation, Cell Line, Tumor, Mitogen-Activated Protein Kinase 3, alpha-2-HS-Glycoprotein
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