Glibenclamide Acts as an Inhibitor of Acyl-CoA:Cholesterol Acyltransferase Enzyme
Biochemical and Biophysical Research Communications, ISSN: 0006-291X, Vol: 277, Issue: 2, Page: 417-422
2000
- 19Citations
- 8Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations19
- Citation Indexes19
- 19
- CrossRef15
- Captures8
- Readers8
Article Description
Sulfonylureas are used in the treatment of non-insulin-dependent diabetes mellitus. Little is known, however, about their effects on cholesterol metabolism. We tested in the present study the effects of glibenclamide (GB) on cholesterol esterification (CE) in macrophage-derived cells. GB inhibited intracellular accumulation of CE induced by acetylated LDL or oxidized LDL in J774 cells, but no such effect on total cholesterol, suggesting that the target of GB was acyl-CoA:cholestrol acyltransferase (ACAT). In the cell-free reconstitution ACAT assay, GB inhibited the ACAT activity with an IC 50 value of 20 μM. Furthermore, GB effectively inhibited the ACAT activity of PMA-stimulated THP-1 cells to the undifferentiated level of THP-1. In the whole-cell ACAT assay using CHO cells overexpressed with ACAT-1 or ACAT-2, GB inhibited the activity of both isozymes with similar potency. Our in vitro data suggest that sulfonylurea could be a potential seed for a new generation of ACAT inhibitors.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0006291X00936817; http://dx.doi.org/10.1006/bbrc.2000.3681; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0034703635&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/11032738; https://linkinghub.elsevier.com/retrieve/pii/S0006291X00936817; https://dx.doi.org/10.1006/bbrc.2000.3681
Elsevier BV
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