Cellular Metabolism and Apoptosis: Dexamethasone, a Promising new Candidate to 
Intervene on the Metabolic Level

Gottschalk, S; Hohnholt, M; Leibfritz , D; Bilodeau, M; Zwingmann, C

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Cellular Metabolism and Apoptosis: Dexamethasone, a Promising new Candidate to Intervene on the Metabolic Level

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https://cds.ismrm.org/ismrm-2008/files/1_program.pdf
(Abstract)

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Gottschalk, S., Hohnholt, M., Leibfritz, D., Bilodeau, M., & Zwingmann, C. (2008). Cellular Metabolism and Apoptosis: Dexamethasone, a Promising new Candidate to Intervene on the Metabolic Level. Poster presented at 16th Scientific Meeting and Exhibition of the International Society of Magnetic Resonance in Medicine (ISMRM 2008), Toronto, Canada.

Cite as: https://hdl.handle.net/11858/00-001M-0000-0013-C993-2

Abstract

Apoptosis – a regulated form of cell death – is the main mode of cell death in most liver injuries. Mitochondria, besides their recognized role as energy-providing metabolic centers, are also key regulatory centers during the genesis of apoptosis. Consequently, increasing interest has developed around the relations between cell metabolism and cell death/survival. We have recently shown that
the initial phase of the apoptotic process is associated with alterations in specific glucose metabolic pathways.
The synthetic glucocorticoid Dexamethasone (DEX) is a commonly used therapeutic agent in several inflammatory disorders.
Besides its clinical use, DEX is known to inhibit apoptosis in vitro. So far, the exact underlying mechanisms of the anti-apoptotic effect of DEX are poorly understood and are currently being investigated.[1,2] Interestingly, with regards to our earlier observations DEX has been shown to modify metabolic pathways (in particular, anaplerosis and gluconeogenesis) both in vivo and in vitro.