Excessive sugar consumption can promote inflammatory processes in the body and facilitate the development of autoimmune diseases.
People who consume too much sugar and other carbs over a lengthy period of time are more likely to acquire autoimmune diseases. The immune system assaults the body’s own tissue in affected patients, resulting in chronic inflammatory bowel illnesses such as Crohn’s disease and ulcerative colitis, type 1 diabetes, and chronic thyroid gland inflammation. The molecular processes that drive autoimmune disorders are multifaceted and intricate.
Scientists at Würzburg’s Julius Maximilians University (JMU) have now deciphered additional details about these processes. Their findings back up the idea that a high-glucose diet increases the pathogenic actions of immune system cells and, conversely, that a low-calorie diet can help with immunological illnesses. They also suggested additional targets for therapeutic approaches based on their findings. Excessive immunological reactions can be suppressed by blocking glucose-dependent metabolic pathways in these immune cells.
Dr. Martin Väth is in charge for the study, now published in Cell Metabolism.
Väth elucidated: “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.”
Väth has showed that an exact glucose transporter or GLUT3, fulfills further metabolic functions in T cells, in addition to generating energy from sugar. In their study, the scientists paid attention on a group of cells of the immune system that have not been known for very long known as Th17 lymphocytes, which play an important role in regulating (auto-) inflammatory processes.
“These Th17 cells express lots of GLUT3 protein on their cell surface,” Väth explains. Glucose is quickly converted to citric acid in the mitochondria before being processed into acetyl-coenzyme A (acetyl-CoA) in the cytoplasm when it is taken in.
Acetyl-CoA plays a role in a variety of metabolic activities, including lipid production. Inflammatory Th17 cells use acetyl-CoA for extra activities. This metabolic intermediate can also affect the activity of other gene segments, according to Väth and his colleagues. As a result, glucose ingestion has a direct impact on pro-inflammatory gene activation.
These novel findings, according to the researchers, pave the path for the creation of targeted therapy for autoimmune illnesses. The dietary supplement Hydroxycitrate, which is used to treat obesity, can decrease the pathogenic functions of Th17 cells. I also reduce the inflammatory-pathological processes by limiting GLUT3-dependent acetyl-CoA production.
The so-called “metabolic reprogramming” of T cells opens up new avenues for treating autoimmune illnesses while preserving the protective roles of immune cells.