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- W2091227895 abstract "Synthetic glucocorticoids are potent anti-inflammatory drugs but show dose-dependent metabolic side effects such as the development of insulin resistance and obesity. The precise mechanisms involved in these glucocorticoid-induced side effects, and especially the participation of adipose tissue in this are not completely understood. We used a combination of transcriptomics, antibody arrays and bioinformatics approaches to characterize prednisolone-induced alterations in gene expression and adipokine secretion, which could underlie metabolic dysfunction in 3T3-L1 adipocytes. Several pathways, including cytokine signalling, Akt signalling, and Wnt signalling were found to be regulated at multiple levels, showing that these processes are targeted by prednisolone. These results suggest that mechanisms by which prednisolone induce insulin resistance include dysregulation of wnt signalling and immune response processes. These pathways may provide interesting targets for the development of improved glucocorticoids." @default.
- W2091227895 created "2016-06-24" @default.
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- W2091227895 date "2013-03-19" @default.
- W2091227895 modified "2023-10-16" @default.
- W2091227895 title "Prednisolone induces the Wnt signalling pathway in 3T3-L1 adipocytes" @default.
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- W2091227895 doi "https://doi.org/10.3109/13813455.2013.774022" @default.
- W2091227895 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3665230" @default.
- W2091227895 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/23506355" @default.
- W2091227895 hasPublicationYear "2013" @default.