Scientists discover how sugar causes inflammation, leading to Crohn’s and other diseases

Too much sugar can lead to inflammation and even trigger the onset of autoimmune diseases. While that may be common knowledge to many scientists, a new study is revealing brand new details about how this process works. The findings may lead to the creation of treatments which prevent conditions such as Crohn’s disease and diabetes.

In the case of autoimmune diseases, a patient’s own defenses attack healthy tissues. Researchers from Julius Maximilians University of Würzburg have found that consuming too much glucose directly impacts the disease-causing functions of certain cells in the immune system.

However, they discovered that a low-calorie diet could have a positive impact on the development of these diseases. The study also identified new targets for therapeutic treatments, such as a blockade of glucose-dependent metabolic processes in the immune cells. This would suppress the immune system from overreacting and causing illness.

“Immune cells need large amounts of sugar in the form of glucose to perform their tasks. With the help of specialized transporters at their cell membrane, they can take up glucose from the environment,” says Dr. Martin Väth in a university release.

Here’s what goes wrong when you eat sugar

Väth’s team demonstrated that a specific glucose transporter, called GLUT3, performs other metabolic tasks inside T cells, besides creating energy from sugar. T cells are an important part of the immune system which help fight off infections. They even appear to help fight off cancer.

Study authors focused on a relatively new group of immune cells: type 17 T helper cells, or Th17 lymphocytes. Recent studies show that these cells play a key role in regulating inflammatory processes in the body.

“These Th17 cells express lots of GLUT3 protein on their cell surface,” Väth explains.

When someone consumes sugar, the powerplants of cells (mitochondria) convert that glucose into citric acid. From there, it is metabolized into acetyl-coenzyme A (acetyl-CoA) inside the gelatinous liquid of the cell (cytoplasm). Acetyl-CoA is an ingredient in many metabolic processes, including the production of lipids.

However, the study finds acetyl-CoA also “fulfills additional functions in inflammatory Th17 cells.” Additionally, Väth’s team showed that acetyl-CoA can regulate the activity of several genes. Therefore, consuming more glucose increases its impact on pro-inflammatory genes.

Thanks to these findings, researchers say blocking GLUT3-dependent synthesis of acetyl-CoA can prevent inflammation and disease-causing functions within immune cells from starting. The team believes the dietary supplement hydroxycitrate, an obesity treatment, is capable of doing this.

The findings are published in the journal Cell Metabolism.

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