Researchers at the Champalimaud Foundation have discovered that the immune system plays a crucial role in regulating blood sugar levels, which may lead to new treatments for diabetes, obesity, and cancer. This finding, published in Science, shifts the focus of immunology from solely combating infections to understanding its broader functions.
Traditionally, blood sugar regulation has been attributed to insulin and glucagon hormones produced by the pancreas. Insulin lowers blood sugar by promoting cellular absorption, while glucagon raises it by signaling the liver to release stored glucose.
The study reveals that immune interactions, particularly between the nervous and immune systems, contribute to blood sugar regulation. Experiments with genetically modified mice lacking a specific immune cell type, ILC2, showed that these mice could not produce sufficient glucagon, resulting in dangerously low glucose levels.
Transplanting ILC2 cells into these mice restored normal blood sugar levels, confirming their role in glucose stabilization during energy scarcity. The researchers initially believed that the immune system regulated glucagon in the liver. However, they found that immune cells travel to the pancreas, releasing cytokines that instruct pancreatic cells to produce glucagon.
Blocking these cytokines led to decreased glucagon levels, underscoring their importance in maintaining blood sugar balance. This study is significant as it demonstrates the first evidence of a nervous-immune-hormonal circuit working together to produce glucose when energy is low.
The implications of this research extend to understanding pancreatic and liver cancers, as well as obesity and diabetes prevention. The communication between body systems observed in mice may also occur in humans during fasting or exercise, paving the way for enhanced therapies in oncology, hormonal, and metabolic disorders.