Danger for sweet tooth
Excessive sugar consumption causes the immune system to attack its own body
Daniil Sukhinov, Naked Science
People who consume sugar and other carbohydrates in excess for a long period of time have an increased risk of developing autoimmune diseases. The immune system of such patients attacks the body's own cells, causing, for example, chronic inflammatory bowel diseases, thyroid gland and type I diabetes. A study by German scientists will help identify new targets for the treatment of a number of similar diseases.
Visualization of a high level of expression of the transmembrane protein GLUT3 in T cells. GLUT3 is colored green, mitochondria – purple, nucleus – blue.
The molecular mechanisms underlying autoimmune diseases are multi-layered and complex. In their study, scientists from the Julius and Maximilian University of Würzburg (Germany) managed to decipher new details of these processes. Their work, published in the journal Cell Metabolism (Hochrein et al., The glucose transporter GLUT3 controls T helper 17 cell responses through glycolytic-epigenetic reprogramming), supports the widespread notion that excessive consumption of glucose and other carbohydrates directly contributes to the development of pathogenic functions in cells of the immune system, and, conversely, that low-calorie diet can help in the treatment of immune diseases.
Together with his team, Dr. Martin Väth from the Institute of Systemic Immunology at the University of Würzburg showed the special role of a specific glucose transporter protein GLUT3, located in the membrane of many cells, in particular immune cells. Scientists have found that in immune T-cells, this protein performs, in addition to the main function — the transfer of glucose into the cell for energy production — additional regulatory functions.
T cells, or T lymphocytes, play an important role in the acquired immune response by recognizing and destroying cells carrying foreign antigens. Scientists focused on a certain group of T cells - type 17 T helper cells, also called Th17 lymphocytes, discovered not so long ago, which play an important role in the regulation of inflammatory and autoinflammatory processes. The main task of T-helpers is to recognize threats and strengthen the immune response by activating other immune cells of the body.
"Th17 cells usually express a large amount of the GLUT3 protein by embedding it in their membrane," explains Dr. Vat. After absorption by the GLUT3 protein, glucose, after undergoing a series of reactions in the mitochondria and cytoplasm of cells, finally turns into an important compound for any cell — acetyl-coenzyme A (acetyl-CoA). Acetyl-CoA, in turn, participates in many metabolic processes (including energy production), and in immune inflammatory cells Th17 performs additional regulatory functions.
A brief description of the mechanism by which increased glucose intake can lead to the development of autoimmune inflammatory processes due to the activation of specialized genes in immune T cells. Figure from the article by Hochrein et al.
Dr. Vet and his team have shown that this metabolic intermediate can also regulate the expression activity of various DNA sites. In particular, acetyl-CoA causes Th17 lymphocytes to produce more pro-inflammatory cytokines — signaling molecules that inform other immune cells about the need to start or intensify the inflammatory process. Thus, excessive glucose consumption leads to an increased accumulation of acetyl-CoA in Th17 lymphocytes, which directly affects the activity of pro-inflammatory genes.
According to the researchers, the data obtained open the way to the development of new approaches to targeted therapy of autoimmune diseases. For example, blocking the GLUT3-dependent synthesis of acetyl-CoA with a dietary supplement — hydroxycitrate, used for the treatment of obesity. This can mitigate the pathogenic functions of Th17 cells and weaken inflammatory and pathological processes by suppressing excessive immune and autoimmune reactions.
The so-called metabolic reprogramming of T cells opens up new possibilities for the treatment of various autoimmune diseases, such as chronic inflammatory bowel diseases (Crohn's disease and ulcerative colitis) and thyroid gland, as well as type I diabetes mellitus (in which insulin-producing cells are destroyed) without reducing the protective functions of immune cells.
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