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  • Perspective
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Circadian rhythms and the gut microbiota: from the metabolic syndrome to cancer

Abstract

The metabolic syndrome is prevalent in developed nations and accounts for the largest burden of non-communicable diseases worldwide. The metabolic syndrome has direct effects on health and increases the risk of developing cancer. Lifestyle factors that are known to promote the metabolic syndrome generally cause pro-inflammatory alterations in microbiota communities in the intestine. Indeed, alterations to the structure and function of intestinal microbiota are sufficient to promote the metabolic syndrome, inflammation and cancer. Among the lifestyle factors that are associated with the metabolic syndrome, disruption of the circadian system, known as circadian dysrhythmia, is increasingly common. Disruption of the circadian system can alter microbiome communities and can perturb host metabolism, energy homeostasis and inflammatory pathways, which leads to the metabolic syndrome. This Perspective discusses the role of intestinal microbiota and microbial metabolites in mediating the effects of disruption of circadian rhythms on human health.

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Fig. 1: The bidirectional bacteria–host relationship.
Fig. 2: Microbiota signalling to the host circadian and metabolic systems occurs via both contact-dependent mechanisms and contact-independent mechanisms.

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Acknowledgements

The authors acknowledge the support provided by NIAAA AA025387 and Rush Translational Sciences Consortium/Swim Across America Organization to F.B., NIAAA AA026801 to A.K. and R.M.V., NIAAA AA023417 and AA026801 to A.K, and NIA AG056653 to R.M.V.. The authors are grateful for the support of the Brinson Foundation, Barbara and Larry Field, Ellen and Philip Glass, and Marcia and Silas Keehn.

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Nature Reviews Endocrinology thanks J. Cryan and the other, anonymous, reviewer(s) for their contribution to the peer review of this work.

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Bishehsari, F., Voigt, R.M. & Keshavarzian, A. Circadian rhythms and the gut microbiota: from the metabolic syndrome to cancer. Nat Rev Endocrinol 16, 731–739 (2020). https://doi.org/10.1038/s41574-020-00427-4

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