Stress Protector

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Science Signaling  15 Jan 2013:
Vol. 6, Issue 258, pp. ec16
DOI: 10.1126/scisignal.2003956

During prolonged fasting, the oxidation of fatty acids leads to increased accumulation of d-β-hydroxybutyrate (βOHB) in the bloodstream. Such increased concentrations of βOHB inhibit class I histone deacetylases. Histone acetylation in turn influences transcriptional activity at various genes. Shimazu et al. (see the Perspective by Sassone-Corsi) found that among the genes showing increased transcription in animals treated with high concentrations of βOHB were two genes implicated in cellular responses to oxidative stress. When treated ahead of time with βOHB, mice were protected from the toxic effects of the oxidative stress causing poison paraquat.

T. Shimazu, M. D. Hirschey, J. Newman, W. He, K. Shirakawa, N. Le Moan, C. A. Grueter, H. Lim, L. R. Saunders, R. D. Stevens, C. B. Newgard, R. V. Farese Jr., R. de Cabo, S. Ulrich, K. Akassoglou, E. Verdin, Suppression of oxidative stress by β-hydroxybutyrate, an endogenous histone deacetylase inhibitor. Science 339, 211–214 (2013). [Abstract] [Full Text]

P. Sassone-Corsi, When metabolism and epigenetics converge. Science 339, 148–150 (2013). [Abstract] [Full Text]

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