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Obesity is driven by a build-up of molecular mesh around hunger neurons

The accumulation of a network of proteins and sugars called the extracellular matrix stops insulin from reaching hunger-regulating neurons, disrupting normal food intake and metabolism, and contributing to obesity.
  1. Alexander Dityatev

    1. Alexander Dityatev is in the German Center for Neurodegenerative Diseases (DZNE), Magdeburg 39120, Germany.

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After eating a meal, the concentration of glucose in the blood rises and triggers β-cells in the pancreas to secrete more of the hormone insulin, which circulates in the blood and reaches the brain. A region of the brain called the arcuate nucleus of the hypothalamus (ARC) is responsible for sensing insulin levels, adjusting food intake and controlling related physiological processes such as burning fat and expending energy. If neurons in the ARC lose sensitivity to insulin, we start to eat more, accumulate fat and develop problems with our metabolic health. Writing in Nature, Beddows et al.1 report that a build-up of a molecular meshwork called the extracellular matrix around neurons stops insulin from reaching its receptor, driving insulin resistance in the brains of obese mice. Freeing neurons from this meshwork restores insulin signalling and drastically reduces body weight.

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Nature 633, 771-772 (2024)

doi: https://doi.org/10.1038/d41586-024-02325-5

References

  1. Beddows, C. A. et al. Nature 633, 914–922 (2024).

    Article  Google Scholar 

  2. Ulbrich, P., Khoshneviszadeh, M., Jandke, S., Schreiber, S. & Dityatev, A. Eur. J. Neurosci. 53, 3811–3830 (2021).

    Article  PubMed  Google Scholar 

  3. Ramsaran, A. I. et al. Science 380, 543–551 (2023).

    Article  PubMed  Google Scholar 

  4. Mirzadeh, Z. et al. Nature Metab. 1, 212–221 (2019).

    Article  PubMed  Google Scholar 

  5. Zhang, X. et al. Cell 135, 61–73 (2008).

    Article  PubMed  Google Scholar 

  6. Kang, L. et al. Diabetes 62, 1888–1896 (2013).

    Article  PubMed  Google Scholar 

  7. Keough, M. B. et al. Nature Commun. 7, 11312 (2016).

    Article  PubMed  Google Scholar 

  8. Lupori, L. et al. Cell Rep. 42, 112788 (2023).

    Article  PubMed  Google Scholar 

  9. Chen, W., Cai, W., Hoover, B. & Kahn, C. R. Trends Neurosci. 45, 384–400 (2022).

    Article  PubMed  Google Scholar 

  10. Riga, D. et al. Sci. Transl. Med. 9, eaai8753 (2017).

    Article  PubMed  Google Scholar 

  11. Stephenson, E. L. et al. Brain 141, 1094–1110 (2018).

    Article  PubMed  Google Scholar 

  12. Tansley, S. et al. Science 377, 80–86 (2022).

    Article  PubMed  Google Scholar 

  13. Blondiaux, A. et al. Neurobiol. Dis. 188, 106324 (2023).

    Article  PubMed  Google Scholar 

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Competing Interests

The author declares no competing interests.

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