Small protein may play a big role in managing type 1 diabetes 20 September 2021 America scientists are hopeful that a small protein may be the key to stopping the autoimmune response that leads to type 1 diabetes. MOTS-c is a small protein that has similar effects on managing blood glucose levels as exercise. Proteins work within cells to build, maintain, and replace tissues that make up the body’s muscles, organs, and immune system. MOTS-c is unique among proteins, as it is encoded in the mitochondria—the area of the cell responsible for converting food into usable energy. MOTS-c promotes the use of glucose for energy and improves the body’s sensitivity to insulin. A new study at the University of Southern California shows that MOTS-c also plays a significant role in regulating the immune system. Type 1 diabetes develops following an autoimmune response that attacks and destroys insulin-producing cells. MOTS-c treatment was found to prevent this autoimmune attack in mice predisposed to develop type 1 diabetes. “We are able to prevent the onset of type 1 diabetes in mouse models,” said assistant professor and co-author, Dr Lee. “MOTS-c injections seem to tame the immune system and to tell them not to tackle their own cells.” Further studies found that people with type 1 diabetes have much lower levels of MOTS-c in their blood compared to people without diabetes. MOTS-c treatment was found to reduce improper cellular attacks in both people with diabetes and people without diabetes. Dr Lee mentioned that this immune-regulating role of MOTS-c may also have the potential to treat other autoimmune conditions. The full findings of this recent study can be accessed from Cell Reports. Key findings • Small protein MOTS-c has similar blood glucose regulating effects as exercise and holds a significant role in regulating the immune system. • MOTS-c treatment reduces the destruction of insulin-producing cells and improves glucose usage. • MOTS-c treatment may assist in managing other autoimmune conditions beyond type 1 diabetes.