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A group of innate immune cells, known as group 2 lymphoid cells (ILC2), are essential for maintaining a stable metabolism in adipose tissue. Obesity significantly impairs the number and function of ILC2 cells, leading to the progression of metabolism-related inflammation. Until now, it was unknown how ILC2 cells are disrupted in obesity.
Researchers at the University Hospital Bonn (UKB) and the University of Bonn have now discovered in obese mice that the key enzyme in fatty acid biosynthesis, known as acetyl-CoA carboxylase 1 (ACC1), is a crucial regulator for the maintenance and function of ILC2 immune cells in adipose tissue. The Bonn researchers thus provide an explanation for the adverse effects of inhibiting acetyl-CoA carboxylase in obesity. Their findings have now been published in the journal Cell Metabolism.
Recent lifestyle changes, such as reduced physical activity and increased consumption of energy-dense, processed foods, have dramatically increased the prevalence of obesity and diabetes worldwide. Although the development of obesity-related metabolic diseases is complex, it is primarily driven by persistent, low-grade inflammation, known as metaflammation. Adipose tissue harbors a wide variety of immune cells that help balance energy supply, blood glucose levels and lipid metabolism by promoting an anti-inflammatory environment. This balance is disrupted in obesity, leading to fundamental changes in adipose tissue.
ILC2 immune cells are involved in lipid metabolism, using free fatty acids to build cell membranes and promote cell growth.
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