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Diabetes

A mitochondrial origin for inherited diabetes mellitus

Nature Reviews Endocrinology volume 19, page 441 (2023)Cite this article

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Mitochondria are ATP-producing metabolic hubs and regulatory centres for cells. Mitochondria are associated, either directly or indirectly, with almost every disease or physiological dysfunction that is understood at the cellular level. These mitochondrial underpinnings of disease were not always taken as a given; modern understanding of mitochondria and metabolism is built upon work published in the 1990s (and previous supporting literature) linking mitochondrial function and genetics to inherited human diseases. For instance, diabetes mellitus is a prominent endocrine disease that involves whole-body metabolism and mitochondrial dysfunction.

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References

Original article

  • Ballinger, S. W. et al. Maternally transmitted diabetes and deafness associated with a 10.4 kb mitochondrial DNA deletion. Nat. Genet. 1, 11–15 (1992)

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Related articles

  • van den Ouweland, J. M. et al. Mutation in mitochondrial tRNA(Leu)(UUR) gene in a large pedigree with maternally transmitted type II diabetes mellitus and deafness. Nat. Genet. 1, 368–371 (1992)

    Article  PubMed  Google Scholar 

  • van den Ouweland, J. M. et al. Maternally inherited diabetes and deafness is a distinct subtype of diabetes and associates with a single point mutation in the mitochondrial tRNA(Leu(UUR)) gene. Diabetes 43, 746–751 (1994)

    Article  PubMed  Google Scholar 

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Acknowledgements

B.J.B. is supported by the Biological Mechanisms for Healthy Aging (BMHA) Training Grant NIH T32AG066574.

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  1. University of Washington Medical Center, Department of Laboratory Medicine and Pathology, Seattle, WA, USA

    Brandon J. Berry

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  1. Brandon J. Berry
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Correspondence to Brandon J. Berry.

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The author declares no competing interests.

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Berry, B.J. A mitochondrial origin for inherited diabetes mellitus. Nat Rev Endocrinol 19, 441 (2023). https://doi.org/10.1038/s41574-023-00856-x

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  • DOI: https://doi.org/10.1038/s41574-023-00856-x

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