Researchers have identified that blocking an enzyme known as CaMKK2 (calcium/calmodulin-dependent protein kinase kinase 2) in immune cells may help prevent obesity, diabetes, and fatty liver disease linked to high-fat diets.
According to a statement released by Monash University, CaMKK2 plays a dual role in regulating how the body uses energy and in controlling inflammation through macrophages—immune cells found in tissues across the body.
A collaborative study involving Australian and U.S. scientists found that mice genetically modified to lack CaMKK2 in their macrophages were shielded from diet-induced obesity and related metabolic complications.
Lead researcher John Scott, from the Monash Institute of Pharmaceutical Sciences, explained that the absence of CaMKK2 caused fat tissue to behave differently. “When the CaMKK2 gene is removed from certain immune cells, fat tissue reprograms itself in a healthier way. The genes begin to support improved metabolism and reduced inflammation,” he said.
The findings, published in Molecular Metabolism, show that CaMKK2 directly influences both immune cell behavior and whole-body metabolism. Researchers say this positions the enzyme as a potential therapeutic target for developing new treatments for obesity and metabolic diseases.