Comorbidities of Diabetes Mellitus and Tuberculosis

The coexistence of diabetes mellitus and tuberculosis represents a synergistic global health challenge. Diabetes increases the risk of developing active tuberculosis by approximately three- to four-fold, while tuberculosis infection can exacerbate glycaemic control. Chronic hyperglycaemia impairs both innate and adaptive immune functions, leading to delayed pathogen clearance, heightened inflammation and more severe pulmonary pathology. Conversely, the systemic inflammation of tuberculosis can induce stress-related hyperglycaemia and unmask pre-existing metabolic dysregulation. This bidirectional interplay contributes to diagnostic delays, poorer treatment outcomes and higher rates of relapse and mortality. The dual burden is most pronounced in regions with high prevalence of both conditions, placing additional strain on health systems. Integrated screening and management strategies that address glycaemic control, nutritional status and host immune responses are emerging as critical components of effective care.

Research from Nature Portfolio

Studies in a murine model of type 2 diabetes have revealed that elevated plasma glycerol—arising from insulin resistance and adipose tissue lipolysis—serves as an auxiliary carbon source for Mycobacterium tuberculosis. In these animals, hyperglycaemia both compromised macrophage function and provided an abundant nutrient reservoir, resulting in increased bacterial burden, exacerbated lung pathology and higher mortality. Utilisation of a glycerol-kinase-deficient mycobacterial strain confirmed that glycerol metabolism directly contributes to susceptibility in the context of type 2 diabetes, highlighting a novel metabolic axis linking host dysmetabolism to pathogen virulence.

Comorbidities of Diabetes Mellitus and Tuberculosis publication trend

The graph below shows the total number of articles in comorbidities of diabetes mellitus and tuberculosis across all publications each year (not limited to Nature Index journals).

Technical terms

Innate immunity: The non-specific, first-line defence mechanisms including phagocytes and complement.

Glycaemic control: Regulation of blood glucose levels, often monitored via glycated haemoglobin (HbA1c).

Latent tuberculosis infection (LTBI): A state in which Mycobacterium tuberculosis persists without causing active disease.

Transcriptome: The full set of RNA transcripts produced by the genome under specific conditions.

Pro-inflammatory cytokines: Signalling molecules that promote inflammation, such as tumour necrosis factor and interleukins.

References

1. Impact of diabetes mellitus on tuberculosis prevention, diagnosis, and treatment from an immunologic perspective. Exploration (2024).
2. Glycerol contributes to tuberculosis susceptibility in male mice with type 2 diabetes. Nature Communications (2023).
3. Impaired resolution of blood transcriptomes through tuberculosis treatment with diabetes comorbidity. Clinical and Translational Medicine (2023).
4. Immunologic, metabolic and genetic impact of diabetes on tuberculosis susceptibility. Frontiers in Immunology (2023).
5. Effect of complicated, untreated and uncontrolled diabetes and pre‐diabetes on treatment outcome among patients with pulmonary tuberculosis. Respirology (2024).
6. Diabetes Mellitus Increases the Risk of Active Tuberculosis: A Systematic Review of 13 Observational Studies. PLOS Medicine (2008).