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NO link between calorie restriction and mitochondria

Nature Chemical Biology volume 1, pages 355–356 (2005)Cite this article

Sir2 is a key regulator in promoting longevity in response to a low-calorie diet. A new role for nitric oxide in promoting mitochondrial synthesis may be the reason why.

A diet low in calories termed calorie restriction (CR) has been known for 70 years to extend mammalian life span1. Recent studies in lower organisms have suggested that the benefits of CR are regulated by the NAD-dependent deacetylase Sir2 (ref. 2), a longevity-promoting gene3. In a recent report in Science, Nisoli et al.4 now provide evidence that levels of the endothelial nitric oxide synthase (eNOS) increase during CR in mice and that this increase mediates an intriguing physiological response to CR—an increase in mitochondrial components and respiration. The new findings are important because CR is still the best-characterized and most robust intervention that can extend mammalian life span.

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Figure 1: In white adipose tissue and other mouse tissues, caloric restriction (CR) induces cGMP production through an increase in eNOS levels.

Rebecca Henretta

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  1. Department of Biology, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, 02139, Massachusetts, USA

    Leonard Guarente

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  1. Leonard Guarente
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Guarente, L. NO link between calorie restriction and mitochondria. Nat Chem Biol 1, 355–356 (2005). https://doi.org/10.1038/nchembio1205-355

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  • DOI: https://doi.org/10.1038/nchembio1205-355

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