Scientists have found that tuberculosis interferes with how glucose is processed in the body.
Researchers from the University of Leicester have found that tuberculosis disrupts glucose metabolism in the body.
The results, now shared in PLoS Pathogens, add to the knowledge that diabetes can intensify tuberculosis symptoms. Notably, they suggest that undiagnosed tuberculosis may lead at-risk patients towards developing metabolic conditions like diabetes.
Tuberculosis (TB) is a bacterial infection that spreads through inhaling tiny droplets released from the lungs of someone who is infected. Although it can affect various parts of the body, it primarily targets the lungs and is one of the most lethal infectious diseases globally, claiming over 4,000 lives daily.
The World Health Organisation prioritizes prevention through the advancement of better vaccines. At present, only one vaccine is available for TB, mainly administered to infants and young children to safeguard them from severe forms of the disease.
The scientists at the university are dedicated to studying tuberculosis with the goal of developing better vaccines, focusing particularly on how undiagnosed and subclinical infections can affect health.
This new discovery may help to identify the molecular mechanisms by which the immune response alters liver metabolism, thereby enabling the development of targeted therapies.
Professor Andrea Cooper, a member of the Leicester Tuberculosis Research Group (LTBRG), is among the paper’s authors.
She mentioned, “Our research shifts the perspective from diabetes worsening TB to the idea that delayed diagnosis of TB might disrupt glucose metabolism, leading to insulin resistance and potentially advancing diabetes in susceptible individuals.”
“Since diabetes complicates drug treatment, our findings further emphasize the necessity for metabolic screenings in any drug or vaccine trials.”
The study initially employed lab models of pulmonary TB to analyze the changes occurring in the liver during the early infection stages. It discovered that an immune reaction was activated within liver cells, resulting in alterations to glucose metabolism.
The lead author, Dr. Mrinal Das, then re-examined existing metabolic data from humans, revealing that liver glucose metabolism was also disrupted in individuals who transitioned from latent TB to active infection.
Professor Cooper added, “Our future goal is to detail the molecular pathways where the immune response modifies liver metabolism, allowing us to potentially establish targeted interventions.”
“We will also be looking into how latent TB—an infection with the TB bacteria that shows no significant symptoms—might affect metabolic health in humans.”
