'Switching Off' Enzyme in Immune Cells May Prevent Obesity and Metabolic Disorders

An international research team led by Monash University and Baylor College of Medicine in Texas has identified a promising target for preventing obesity and related metabolic diseases. They discovered that inhibiting an enzyme called CaMKK2 within immune cells, specifically macrophages, can effectively protect against diet-induced obesity, insulin resistance, fatty liver disease, and other metabolic complications.

CaMKK2 (Calcium/calmodulin-dependent protein kinase kinase 2) plays a crucial role in regulating cellular energy use and inflammation, especially in macrophages—immune cells present throughout tissues that communicate inflammatory signals. In their study, scientists genetically modified mice so their macrophages lacked CaMKK2. These mice demonstrated notable resistance to the negative effects of a high-fat diet, including reduced fat accumulation and improved metabolic health.

Dr. John Scott from Monash University explained that CaMKK2 is a key regulator of how macrophages influence metabolism and inflammation. Under stress conditions like a high-fat diet, macrophages tend to become inflammatory, contributing to the development of obesity and insulin resistance. The research revealed that removing CaMKK2 from immune cells shifts fat tissue behavior toward a healthier state, enhancing metabolic gene activity and reducing harmful inflammation.

Professor Anthony Means from Baylor College of Medicine highlighted that CaMKK2 functions as a molecular switch that controls macrophage metabolism and inflammation, linking metabolic processes to immune responses. This understanding opens avenues for new therapies targeting CaMKK2 to treat obesity and metabolic syndrome.

Overall, this research suggests that inhibiting CaMKK2 could be a viable strategy to combat obesity-related health issues by modulating immune cell function and promoting healthier metabolism.