Circumventing the Crabtree effect: replacing media glucose with galactose increases susceptibility of HepG2 cells to mitochondrial toxicants.

By Lisa D. Marroquin, J. Hynes, J. Dykens, J. Jamieson, Y. Will. Toxicological Sciences, 2007

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The Mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance (2015, positive): “In mammalian cells, galactose is largely metabolized by the mitochondria (Marroquin et al., 2007).”
Cisplatin Induces a Mitochondrial-ROS Response That Contributes to Cytotoxicity Depending on Mitochondrial Redox Status and Bioenergetic Functions (2013, result): “Such a metabolic adaptation results in lower susceptibility toward the effects of mitochondrial toxicants on cell viability and growth [64]; therefore, the contribution of cisplatin-induced mitochondrial impairment to its cytotoxic effect may have been underestimated in our study as well as in those”
Circadian Clock NAD+ Cycle Drives Mitochondrial Oxidative Metabolism in Mice (2013, background): “Consistent with impaired mitochondrial energy production from FAO, MEFs lacking the clock activator Bmal1 produced ~30% less adenosine triphosphate (ATP) when maintained in medium containing galactose, which shifts ATP production from glycolysis to mitochondrial oxidative metabolism (19).”
SIRT3 opposes reprogramming of cancer cell metabolism through HIF1α destabilization (2011, background): “To test whether this increased growth rate required aerobic metabolism of glucose, we grew cells in media containing galactose instead of glucose, thereby reducing glycolytic flux and forcing the cell to rely on mitochondrial oxidative phosphorylation (Marroquin et al., 2007).”