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Glycerol contributes to tuberculosis susceptibility in male mice with type 2 diabetes

Author

Listed:
  • Nuria Martinez

    (University of Massachusetts Chan Medical School)

  • Lorissa J. Smulan

    (University of Massachusetts Chan Medical School)

  • Michael L. Jameson

    (University of Massachusetts Chan Medical School)

  • Clare M. Smith

    (University of Massachusetts Chan Medical School)

  • Kelly Cavallo

    (University of Massachusetts Chan Medical School)

  • Michelle Bellerose

    (University of Massachusetts Chan Medical School)

  • John Williams

    (University of Massachusetts Chan Medical School)

  • Kim West

    (University of Massachusetts Chan Medical School)

  • Christopher M. Sassetti

    (University of Massachusetts Chan Medical School)

  • Amit Singhal

    (University of Massachusetts Chan Medical School
    A*STAR Infectious Diseases Labs (ID Labs), Agency for Science, Technology and Research (A*STAR)
    Singapore Immunology Network (SIgN), Agency for Science, Technology and Research (A*STAR)
    Nanyang Technological University)

  • Hardy Kornfeld

    (University of Massachusetts Chan Medical School)

Abstract

Diabetes mellitus increases risk for tuberculosis disease and adverse outcomes. Most people with both conditions have type 2 diabetes, but it is unknown if type 1 and type 2 diabetes have identical effects on tuberculosis susceptibility. Here we show that male mice receiving a high-fat diet and streptozotocin to model type 2 diabetes, have higher mortality, more lung pathology, and higher bacterial burden following Mycobacterium tuberculosis infection compared to mice treated with streptozotocin or high-fat diet alone. Type 2 diabetes model mice have elevated plasma glycerol, which is a preferred carbon source for M. tuberculosis. Infection studies with glycerol kinase mutant M. tuberculosis reveal that glycerol utilization contributes to the susceptibility of the type 2 diabetes mice. Hyperglycemia impairs protective immunity against M. tuberculosis in both forms of diabetes, but our data show that elevated glycerol contributes to an additional adverse effect uniquely relevant to type 2 diabetes.

Suggested Citation

  • Nuria Martinez & Lorissa J. Smulan & Michael L. Jameson & Clare M. Smith & Kelly Cavallo & Michelle Bellerose & John Williams & Kim West & Christopher M. Sassetti & Amit Singhal & Hardy Kornfeld, 2023. "Glycerol contributes to tuberculosis susceptibility in male mice with type 2 diabetes," Nature Communications, Nature, vol. 14(1), pages 1-11, December.
  • Handle: RePEc:nat:natcom:v:14:y:2023:i:1:d:10.1038_s41467-023-41519-9
    DOI: 10.1038/s41467-023-41519-9
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    References listed on IDEAS

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    1. Kevin Pethe & Patricia C. Sequeira & Sanjay Agarwalla & Kyu Rhee & Kelli Kuhen & Wai Yee Phong & Viral Patel & David Beer & John R. Walker & Jeyaraj Duraiswamy & Jan Jiricek & Thomas H. Keller & Arnab, 2010. "A chemical genetic screen in Mycobacterium tuberculosis identifies carbon-source-dependent growth inhibitors devoid of in vivo efficacy," Nature Communications, Nature, vol. 1(1), pages 1-8, December.
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    Cited by:

    1. Yi Lei & Qiangyun Liu & Binggui Chen & Fangfang Wu & Yiming Li & Xue Dong & Nina Ma & Ziru Wu & Yanfang Zhu & Lu Wang & Yuxin Fu & Yuming Liu & Yinting Song & Mei Du & Heng Zhang & Jidong Zhu & Timoth, 2024. "Protein O-GlcNAcylation coupled to Hippo signaling drives vascular dysfunction in diabetic retinopathy," Nature Communications, Nature, vol. 15(1), pages 1-23, December.

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