In a groundbreaking study published in PLoS Pathogens, researchers from the University of Leicester have unveiled new insights into the interrelation between tuberculosis (TB) and diabetes, significantly enhancing the understanding of how each condition can influence the other. This research complements existing knowledge that diabetes exacerbates TB symptoms but crucially suggests that undiagnosed TB may also predispose individuals to metabolic disorders such as diabetes.
TB, a bacterial infection primarily impacting the lungs, is a major global health challenge, causing over 4,000 fatalities daily. The disease's spread is facilitated by inhaling droplets from an infected individual. Despite its lethality, TB prevention relies heavily on a single vaccine administered mainly to infants and young children. This limited preventive measure underscores the World Health Organisation's prioritization of developing improved vaccines.
The University of Leicester's research team is actively engaged in tuberculosis research, seeking to develop more effective vaccines. Their focus is on understanding how undiagnosed and subclinical TB infections can affect overall health. Their recent discovery could unlock the molecular pathways by which immune responses alter liver metabolism, a finding that holds potential for creating targeted therapeutic interventions.
Professor Andrea Cooper, a key contributor to the study as part of the Leicester Tuberculosis Research Group (LTBRG), emphasized a pivotal shift in focus their research brings. "Our paper changes the focus from diabetes making TB worse to the possibility that late diagnosis of TB can contribute to disruption of glucose metabolism, insulin resistance and therefore can promote progress towards diabetes in those that are susceptible," she explained. These revelations underline the necessity for metabolic screening in conjunction with any TB drug or vaccine trials, given that diabetes can compromise treatment efficacy.
The study initially employed laboratory models to scrutinize the liver's response in early TB infection stages, revealing that the liver's immune response can disrupt glucose metabolism. Dr. Mrinal Das, the study's primary author, further validated these findings through the reanalysis of human metabolic data, showing similar disruptions in glucose metabolism when latent TB progressed to active TB.
Looking ahead, Professor Cooper stressed the importance of elucidating the molecular mechanisms behind immune-induced metabolic changes in the liver. This knowledge could facilitate the development of precise interventions. Furthermore, the team aims to explore how latent TB infection—characterized by the presence of TB bacteria without overt symptoms—affects metabolic health in humans.
This pioneering research not only advances our understanding of TB and its intersection with metabolic health but also highlights the potential for innovative therapeutic strategies to mitigate the dual burden of tuberculosis and diabetes.
