ArticleLipids in health and disease2015
Mechanism of the effect of glycosyltransferase GLT8D2 on fatty liver.
Article in Lipids in health and disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04081571 (Prevalence of NAFLD and Correlation With Its Main Risk Factors Among Egyptian Multicenter National Study), which is not on this map. Cited by 12 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Prevalence of NAFLD and Correlation With Its Main Risk Factors Among Egyptian Multicenter National Study
Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- FOXQ1 activates GLT8D2 to enhance CCL2 N-glycosylation and promote prostate cancer bone metastasis.Cell death & disease · 2026Article
- GLT8D2 is a prognostic biomarker and regulator of immune cell infiltration in gastric cancer.Frontiers in immunology · 2024Article
- Glycosyltransferase GLT8D1 and GLT8D2 serve as potential prognostic biomarkers correlated with Tumor Immunity in Gastric Cancer.BMC medical genomics · 2023Article
- Overexpression of glycosyltransferase 8 domain containing 2 confers ovarian cancer to CDDP resistance by activating FGFR/PI3K signalling axis.Oncogenesis · 2021Article
- Systems genetics in diversity outbred mice inform BMD GWAS and identify determinants of bone strength.Nature communications · 2021Article
- Article
- A genomic variant of ALPK2 is associated with increased liver fibrosis risk in HIV/HCV coinfected women.PloS one · 2021Article
- GLT25D2 Is Critical for Inflammatory Immune Response to Promote Acetaminophen-Induced Hepatotoxicity by Autophagy Pathway.Frontiers in pharmacology · 2020Article
- Comparative Analysis of MicroRNA and mRNA Profiles of Sperm with Different Freeze Tolerance Capacities in Boar (Biomolecules · 2019Article
- HO-1/EBP interaction alleviates cholesterol-induced hypoxia through the activation of the AKT and Nrf2/mTOR pathways and inhibition of carbohydrate metabolism in cardiomyocytes.International journal of molecular medicine · 2017Article
- Glycosyltransferases and non-alcoholic fatty liver disease.World journal of gastroenterology · 2016Review
- Bacterial Glycosyltransferases: Challenges and Opportunities of a Highly Diverse Enzyme Class Toward Tailoring Natural Products.Frontiers in microbiology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRecent studies have shown that some glycosyltransferases are involved in the development of nonalcoholic fatty liver disease (NAFLD). The objective of this study was to explore the effect and mechanism of glycosyltransferase GLT8D2 on fatty liver.
methodsRat model of NAFLD was established by induction with high-fat-diet. The GLT8D2 expression in rat liver was examined using immunohistochemistry. Oil Red O staining and triglyceride assay were used to measure the effect of abnormal GLT8D2 expression on lipid accumulation in HepG2 cells. The expression levels of lipid metabolism-related key molecules, namely sterol regulatory element-binding protein-1c (SREBP-1c), stearoyl-coA desaturase (SCD), carnitine palmitoyltransferase-1 (CPT1) and microsomal triglyceride transfer protein (MTP), in HepG2 cells with abnormal GLT8D2 expression were determined by western blot analyses.
resultsThe expression of GLT8D2 was higher in the liver of rats with NAFLD than in the control rats, and GLT8D2 was mainly located around lipid droplets in hepatocytes. GLT8D2 expression increased in steatosis HepG2 cells compared with that in normal HepG2 cells. GLT8D2 positively regulated lipid droplet accumulation and triglyceride content in HepG2 cells. Upregulation or knockdown of GLT8D2 had no effect on the expressions of SREBP-1c, SCD or CPT-1 proteins in HepG2 cells. However, GLT8D2 expression negatively regulated the expression of MTP protein in HepG2 cells.
conclusionGLT8D2 participated in NAFLD pathogenesis possibly by negatively regulating MTP expression. Specific inhibition of GLT8D2 via an antagonistic strategy could provide a potential candidate approach for treatment of NAFLD.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.