The cause–effect relation of tuberculosis on incidence of diabetes mellitus

Abstract

Tuberculosis (TB) is one of the oldest human diseases and is one of the major causes of mortality and morbidity across the Globe. Mycobacterium tuberculosis (Mtb), the causal agent of TB is one of the most successful pathogens known to mankind. Malnutrition, smoking, co-infection with other pathogens like human immunodeficiency virus (HIV), or conditions like diabetes further aggravate the tuberculosis pathogenesis. The association between type 2 diabetes mellitus (DM) and tuberculosis is well known and the immune-metabolic changes during diabetes are known to cause increased susceptibility to tuberculosis. Many epidemiological studies suggest the occurrence of hyperglycemia during active TB leading to impaired glucose tolerance and insulin resistance. However, the mechanisms underlying these effects is not well understood. In this review, we have described possible causal factors like inflammation, host metabolic changes triggered by tuberculosis that could contribute to the development of insulin resistance and type 2 diabetes. We have also discussed therapeutic management of type 2 diabetes during TB, which may help in designing future strategies to cope with TB-DM cases.

Insulin resistance, and not β-cell impairment, mediates association betweenMycobacterium tuberculosissensitization and type II diabetes mellitus among US adults

“…According to the literature, the majority of patients with glucose intolerance during active TB regress to normoglycemia after antituberculosis treatment. 16 Transient hyperglycemia is also seen with other severe systemic infections, such as community-acquired pneumonia, supporting the possibility of a non-specific stress response to infection. 17 Unfortunately, our study lacked follow-up data on the trajectories of M. tb-associated impaired glucose regulation.…”

“…38 Insulin resistance has also been attributed to impaired liver function due to the toxic effect of anti-tuberculosis drugs. 16 Inflammation from M.tb infection results in an environment of sustained pro-inflammatory cytokine production often leading to metabolic dysregulation and eventually insulin resistance. 16 Philips et al ., 2017 in South Africa found insulin resistance in a quarter of newly diagnosed male and female TB patients.…”

“…16 Inflammation from M.tb infection results in an environment of sustained pro-inflammatory cytokine production often leading to metabolic dysregulation and eventually insulin resistance. 16 Philips et al ., 2017 in South Africa found insulin resistance in a quarter of newly diagnosed male and female TB patients. 39 Similarly, we found M.tb sensitization to be associated with greater insulin resistance, which in turn was on the mechanistic pathway to T2DM.…”

“…However, M.tb infection likely has systemic-mediated diabetogenic effects. 16 For example, the proinflammatory cytokine cascade set off by M.tb antigens may drive insulin resistance in skeletal muscle, adipose tissue and liver by adversely altering cellular and intracellular insulin signaling 16, 19, 20 , while islet amyloid deposition associated with M.tb infection may precipitate β-cell failure 18, 19 through loss of both β-cell mass and function. 20 Of note, amyloidosis in tuberculosis is documented in the USA 21 , and tuberculosis is the commonest cause of secondary amyloidosis in LMIC settings.…”

Multivariate regression analysis affecting successful treatment of pulmonary tuberculosis patients in western China: a retrospective study in a high-incidence area

“…Our study identifies prevalent comorbidities such as diabetes, HIV/AIDS, and pneumoconiosis, which significantly impact treatment outcomes. Extensive research underscores the deleterious effect of diabetes on TB treatment outcomes [46][47][48], while the influence of HIV/AIDS on TB is widely acknowledged [49,50]. Additionally, studies elucidate the intricate interaction between pneumoconiosis and PTB treatment [51,52].…”