High-fat diets suppress enzyme in immune cells, promoting fat tissue inflammation in mice
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.
Obese mice exhibit increased fatty acid uptake in their immune cells, leading to the suppression of a crucial enzyme called acetyl-CoA carboxylase 1 (ACC1). This inhibition disrupts the maintenance and function of group 2 lymphoid cells (ILC2) in adipose tissue, contributing to inflammation and enlargement of fat tissue. The research from the University Hospital Bonn and the University of Bonn reveals that ACC1 plays a key role in balancing lipid metabolism and energy production within ILC2 cells.
When mice consume a high-fat diet, the enzyme is inhibited, impairing the cells' ability to produce energy and maintain a healthy inflammatory response. This self-reinforcing mechanism highlights the importance of considering immune cell metabolism in the development of obesity and diabetes treatments.
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