Excessive sugar consumption can promote inflammatory processes in the body and lead to the development of autoimmune diseases.
Individuals consuming sugar and other carbohydrates in excessive amounts over a long period have an increased risk of causing inflammation and developing an autoimmune disease. In affected patients, the immune system attacks the body’s tissue leading to conditions such as Crohn’s disease or type 1 diabetes.
Consuming sugar in excessive amounts can not only lead to autoimmune diseases but can cause weight gain and tooth decay. The UK government recommends that adults should consume no more than 30g of free sugars – sugars added to food or drinks and sugars found naturally in honey, syrups and unsweetened fruit and vegetable juices, smoothies and purees. Additionally, children aged between seven to ten should consume no more than 24 grams and any children aged four to six should have no more than 19 grams.
Dr Martin Väth, responsible for the study which has been published in the journal Cell Metabolism, is a junior research group leader at the Institute of Systems Immunology – a Max Planck research group under the umbrella of JMU that focusses on the interplay of the immune system with the organism.
Consuming sugar excessively and autoimmune disease
The underlying molecular mechanisms that promote autoimmune diseases are multi-layered and complex. Scientists from the Julius Maximilians University of Würzburg (JMU) have uncovered new details of these inflammatory processes. Their findings support the theory that consuming sugar and other glucose forms in excessive amounts directly promotes the pathogenic functions of certain cells of the immune system, and consequently, a reduced-calorie diet could have a beneficial effect on immune diseases. Based on the researchers’ findings, they further identified new targets for therapeutic interventions: a specific blockade of glucose-depended metabolic processes in these immune cells can suppress excessive immune reactions.
Martin Väth explained: “Immune cells need large amounts of sugar in the form of glucose to perform their tasks. With the help of specialised transporters at their cell membrane, they can take up glucose from the environment.”
Together with his team, Väth has shown that a specific glucose transporter – scientifically named GLUT3 – fulfils additional metabolic functions in T cells besides generating energy from consuming sugar.
The scientists carried out their study by focussing on a group of cells of the immune system that have remained unknown until recently: T helper cells of type 17, also 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 explained. Once taken up, glucose is readily converted to citric acid in the mitochondria before it is metabolised into acetyl-coenzyme A (acetyl-CoA) in the cytoplasm. Acetyl-CoA is involved in numerous metabolic processes, including the biosynthesis of lipids.
Influence on pro-inflammatory genes
However, acetyl-CoA fulfils additional functions in inflammatory Th17 cells. Väth and his team showed that this metabolic intermediate can also regulate the activity of various gene segments. Thus, glucose consumption has a direct influence on the activity of pro-inflammatory genes.
According to the researchers, these new findings pave the way for the development of targeted therapy of autoimmune diseases. For example, blocking GLUT3-dependent synthesis of acetyl-CoA by the dietary supplement hydroxycitrate, which is used to treat obesity, can mitigate the pathogenic functions of Th17 cells and reduce inflammatory-pathological processes. The so-called “metabolic reprogramming” of T cells opens new possibilities to treat autoimmune diseases without curtailing protective immune cell functions.
