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

Nuria Martinez, Lorissa J. Smulan, Michael L. Jameson, Clare M. Smith, Kelly Cavallo, Michelle Bellerose, John Williams, Kim West, Christopher M. Sassetti, Amit Singhal and Hardy Kornfeld ()
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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
Hardy Kornfeld: University of Massachusetts Chan Medical School

Nature Communications, 2023, vol. 14, issue 1, 1-11

Abstract: 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.

Date: 2023
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DOI: 10.1038/s41467-023-41519-9

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