How sugar promotes inflammation

People who consume a lot of sugar and other sugars over a long period of time have a higher risk of developing an autoimmune disease. The immune system attacks the body's own tissue in affected patients, and the consequences are chronic inflammatory bowel diseases, such as Crohn's disease and ulcerative colitis, type 1 diabetes and chronic inflammation of the thyroid gland.

There are new targets for therapy.

There are many mechanisms that promote autoimmune diseases. Scientists at the JMU have succeeded in understanding new details of these processes. Their work supports the idea that excessive consumption of sugar directly affects the function of certain cells of the immune system and that a reduced diet can have a beneficial effect on immune diseases. They identified new targets for therapeutic interventions based on these findings.

The study was published in the journal Cell Metabolism. The Institute of Systems Immunology is under the umbrella of JMU and focuses on the interplay of the immune system with the organisms. This study was also done by people from other countries.

There is a side job for aglucose transporter.

Immune cells need large amounts of sugar in the form ofglucose to perform their tasks. With the help of specialized transporters at their cell membranes, they can take up glucose from the environment.

The scientists focused on a group of cells of the immune system that have not been known for a long time: T helper cells of type 17, which play an important role in regulating inflammatory processes.

The Th17 cells have lots of GLUT3 on their cell surface. Once taken up, it is easy to convert glucose to acetyl-coenzyme A in the nucleus of the cell. Acetyl-CoA is involved in many metabolism processes.

Influence on pro inflammatory genes.

Th17 cells have additional functions thanks to acetyl-CoA. The team showed that this metabolic intermediate can regulate the activity of various genes. The activity of pro inflammatory genes is influenced by the consumption of sugar.

The new findings pave the way for the development of targeted therapy for autoimmune diseases. Th17 cells can be mitigated and inflammatory-pathological processes can be reduced by blocking GLUT synthesis3- dependent of acetyl-CoA by the diet supplement hydroxycitrate. New possibilities to treat autoimmune diseases without curtailing protective immune cell functions can be found in the so-called "metabolic reprogrammation" of T cells.

The story was told

The materials were provided by the University of rzburg. The original was written by Gunnar Bartsch. Content can be edited for style and length.

Journal reference

1. Sophia M. Hochrein, Hao Wu, Miriam Eckstein, Laura Arrigoni, Josip S. Herman, Fabian Schumacher, Christian Gerecke, Mathias Rosenfeldt, Dominic Grün, Burkhard Kleuser, Georg Gasteiger, Wolfgang Kastenmüller, Bart Ghesquière, Jan Van den Bossche, E. Dale Abel, Martin Vaeth. The glucose transporter GLUT3 controls T helper 17 cell responses through glycolytic-epigenetic reprogramming. Cell Metabolism, 2022; DOI: 10.1016/j.cmet.2022.02.015