Study finds tuberculosis alters liver metabolism and could promote diabetes

Scientists from the University of Leicester have discovered that tuberculosis disrupts glucose metabolism in the body.

The results, which have now been published in PLoS Pathogensadd to the understanding that diabetes worsens the symptoms of tuberculosis. Above all, they now say, undiagnosed tuberculosis could push vulnerable patients toward metabolic diseases such as diabetes.

Tuberculosis (TB) is a bacterial infection that is spread by inhaling tiny droplets from the lungs of an infected person. It can affect any part of the body, but primarily affects the lungs and remains one of the most devastating infectious diseases in the world, killing more than 4,000 people every day.

Prevention through the development of improved vaccines remains a priority for the World Health Organization. Currently, there is only one vaccine against tuberculosis, and it is mainly given to infants and young children to protect them from severe forms of infection.

Scientists at the University are studying tuberculosis in hopes of creating improved vaccines and are specifically studying the ways in which undiagnosed, subclinical infection can impact health. According to them, this new discovery could pave the way for defining the molecular pathways by which the immune response modifies hepatic metabolism, thus allowing the creation of targeted interventions.

Professor Andrea Cooper from the university’s Leicester Tuberculosis Research Group (LTBRG) is among the authors of the paper. She said: “Our paper shifts the focus from diabetes aggravating TB to the possibility that late diagnosis of TB may contribute to disruption of glucose metabolism, insulin resistance and therefore may promote progression towards diabetes in susceptible people.

“As diabetes compromises drug treatment, our paper also supports the idea that metabolic screening should be involved in any drug or vaccine trial.”

The study first used laboratory models of pulmonary tuberculosis to examine changes occurring in the liver during the early stages of infection. It was found that an immune response was triggered within liver cells and glucose metabolism was impaired.

Lead author Dr. Mrinal Das then reanalyzed published metabolic data in humans, where he found that hepatic glucose metabolism was also disrupted when people progressed to tuberculosis following latent infection .

Professor Cooper added: “Our future aim is to define the molecular pathways by which the immune response alters hepatic metabolism, potentially allowing us to create targeted interventions. We will also study how latent tuberculosis (which is an infection with the bacterial agent of tuberculosis without significant symptoms) could impact metabolic health in humans.