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IMMUNOMETABOLISM

Inflammation brakes mitochondrial metabolism in obesity

Nature Immunology volume 21, pages 1143–1145 (2020)Cite this article

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A vicious cycle, linking obesity with chronic inflammation, fuels the development and exacerbation of metabolic syndrome and other disorders. Modulation of mitochondrial energy metabolism via interleukin-1β signaling establishes a runaway positive-feedback loop that brings about and reinforces the sequelae of a high-fat diet.

Obesity is rapidly becoming a global health hazard1. According to the World Health Organization, in recent years, the prevalence of obesity worldwide has reached epidemic proportions2. The societal ramifications of this grim development are wide ranging, given that obesity is also a major risk factor for, and is tightly associated with, devastating human pathologies, including cardiovascular diseases, type 2 diabetes mellitus, cancer, metabolic disorders, dementia and accelerated aging, among others2. Thus, understanding the intricate signaling pathways and molecular mechanisms underlying and sustaining the complex physiology of obesity is becoming a pressing priority.

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Fig. 1: Reprogramming of mitochondrial metabolism.

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Authors and Affiliations

  1. Institute of Molecular Biology and Biotechnology, Foundation for Research and Technology-Hellas, Heraklion, Crete, Greece

    Nektarios Tavernarakis

  2. School of Medicine, University of Crete, Heraklion, Crete, Greece

    Nektarios Tavernarakis

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  1. Nektarios Tavernarakis
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Correspondence to Nektarios Tavernarakis.

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Tavernarakis, N. Inflammation brakes mitochondrial metabolism in obesity. Nat Immunol 21, 1143–1145 (2020). https://doi.org/10.1038/s41590-020-0780-8

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