Altered Systemic Adipokine Levels in Pulmonary Tuberculosis and Changes following Treatment

Abstract

Pulmonary tuberculosis (PTB) is associated with modulation of levels of adipokines, specifically adiponectin and leptin, but the effect of standard antituberculosis treatment (ATT) on the systemic levels of adiponectin, resistin, and leptin has not been well explored. To identify the association of adipokines with PTB and their relationship with disease severity and bacterial burden, we measured the levels of adiponectin, resistin, and leptin in PTB individuals and compared them with latent tuberculosis (LTB) and healthy control (HC) individuals. Pulmonary tuberculosis was characterized by diminished circulating levels of adiponectin and leptin and heightened circulating levels of resistin in comparison to that in LTB and HC individuals. However, PTB with bilateral or cavitary disease did not exhibit any increased systemic levels of these adipokines in comparison with those with unilateral or non-cavitary disease, respectively. In addition, none of the adipokines exhibited a positive correlation with bacterial burdens, but adiponectin alone exhibited a negative correlation with body mass index in PTB individuals. Finally, on successful completion of ATT, PTB individuals exhibited significantly increased levels of adiponectin and leptin and significantly decreased levels of resistin. Therefore, our data identify an important association of systemic adipokine levels with PTB disease and its alteration following ATT.

The association between adipokines and pulmonary diseases: a mendelian randomization study

“…Clinical research has demonstrated that pulmonary tuberculosis is characterized by diminished circulating adiponectin and leptin levels, as well as augmented resistin levels [ 8 ]. Serum adiponectin concentrations have been shown to provide protection against asthma in premenopausal women and adolescent girls [ 34 ].…”

“…Collectively, adipokines may play a crucial role in pulmonary diseases, particularly in the context of inflammatory disorders, malignancies, and interstitial lung diseases. However, the associations between adipokines and interstitial lung disease (ILD) [ 4 ], asthma [ 5 ], chronic obstructive pulmonary disease (COPD) [ 6 ], lung cancer [ 7 ], tuberculosis [ 8 ], sleep apnea syndrome (SAS) [ 9 ], and pneumonia [ 10 ] remain unclear. Causality cannot be deduced from the existing evidence.…”

Hepatitis B Virus and Tuberculosis Are Associated with Increased Noncommunicable Disease Risk among Treatment-Naïve People with HIV: Opportunities for Prevention, Early Detection and Management of Comorbidities in Sierra Leone

“…Diabetics are 1.5 to 3 times more likely to develop active TB [ 63 , 64 ]. Conversely, a meta-analysis by Menon et al [ 65 ] showed that up to 50% of people diagnosed with TB had hyperglycemia at baseline, which remained unresolved in over 10% of cases even after 6 months of effective anti-TB treatment. Although the pathophysiologic basis of hyperglycemia/DM in TB has not been fully elucidated, a role has been postulated for adipokine-mediated alterations in the microenvironment, resulting in increased susceptibility to hyperglycemia through the release of counterregulatory stress hormones (e.g., glucagon, cortisol and growth hormone) [ 66 , 67 ].…”

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

“…TNF-α completely blocks SREBP-1 expression and its activation ( Sewter et al., 2002 ; Das and Mukhopadhyay, 2011 ). Resistin also links to inflammation and higher resistin levels were observed in tuberculosis and T2D patients ( Youn et al., 2004 ; Gharibeh et al., 2010 ; Das and Mukhopadhyay, 2011 ; Moideen et al., 2018 ). Resistin activates pro-inflammatory cytokines like IL-12 and TNF-α through the NF-κB-dependent pathway in mouse and human macrophages and is directly correlated to glucose homeostasis ( Asensio et al., 2004 ; Silswal et al., 2005 ).…”