Autoimmune diseases, too much sugar increases the risk – breaking latest news

Evidence of excessive sugar intake continues to accumulate: research published in Cell Metabolism
by researchers from the University of Wurzburg in Germany recently showed that excess glucose affects a particular subtype of white blood cellsfavoring an increase in inflammation and the subsequent appearance of autoimmune diseasesthose in which the immune system attacks cells and tissues of the body itself and which include diseases such as type 1 diabetes, ulcerative colitis or multiple sclerosis.

Cell study

The data comes from a laboratory investigation on T lymphocytes helper type 17little known but essential for regulating inflammatory and auto-inflammatory processes: these cells have numerous on their surface glucose transportersor proteins that recover sugar molecules from the external environment to bring them inside the cell in order to be used as a source of energy. The cells of the immune system need large amounts of glucose for their complex functions, for which they express many transporters; T helper 17 lymphocytes, in particular, are coated with GLUT3, a subtype of glucose transporter with peculiar characteristics.

Pro-inflammatory genes

Once it enters the immune cells via GLUT3, glucose is transformed through metabolic steps which lead among other things to the production of acetyl-coenzyme Aa molecule involved in countless metabolic pathways, but which plays an additional role in T helper 17 lymphocytes: German researchers have shown that acetyl-coenzyme A it regulates and influences the activity of some pro-inflammatory genes involved in the emergence of autoimmune diseases. An excess of sugar from the diet therefore results in an increase in transcription and therefore in the action of these genes that trigger inflammation.

Metabolic reprogramming

The discovery, in addition to giving one more reason to cut the simple sugars of sweets, cookies and sugary drinkscould open new avenues for the therapy of autoimmune diseases because, as Martin Vath, head of the study, specifies, blocking the production of acetyl-coenzyme A dependent on the GLUT3 transporter through specific molecules could help to obtain a “metabolic reprogramming” of pro-inflammatory lymphocytes involved in the development of autoimmunity, helping to tackle these pathologies without affecting the normal immune response to harmful external agents.