High-fat diets suppress enzyme in immune cells, promoting fat tissue inflammation in mice
· Medical Xpressby University Hospital of Bonn
edited by Gaby Clark, reviewed by Andrew Zinin
Gaby Clark
Scientific Editor
Meet our editorial team
Behind our editorial process
Andrew Zinin
Chief Editor
Meet our editorial team
Behind our editorial process Editors' notes
This article has been reviewed according to Science X's editorial process and policies. Editors have highlighted the following attributes while ensuring the content's credibility:
fact-checked
peer-reviewed publication
trusted source
proofread
The GIST Add as preferred source
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. "Enzymes such as ACC1, which regulate lipid metabolism, could favor the retention of ILC2 cells in lipid-rich environments such as adipose tissue," says Christoph Wilhelm, a professor at the Institute of Clinical Chemistry and Clinical Pharmacology at the UKB. "We found that these immune cells are metabolically impaired in obesity."
Increased fatty acid consumption drives metabolic dysfunction
The enzyme ACC1 is a key regulator of cellular metabolic balance. When fatty acids are scarce, it facilitates the production of long-chain fatty acids within cells. If sufficient fatty acids are present in the environment—for example, as a result of a high-fat diet (HFD)—the enzyme is inhibited to prevent further fat production. This mechanism is useful, but the inhibition impairs the maintenance and function of ILC2 immune cells. That leads to enlargement and inflammation of adipose tissue, predisposing mice to diabetes.
"We found that HFD-induced obesity in mice increases the uptake of fatty acids from the environment. This suppresses the enzyme ACC1 in the ILC2 cells of the adipose tissue," says co-first author Fotios Karagiannis from Wilhelm's research group.
The researchers attribute this effect to a previously unrecognized role of ACC1 in maintaining the citrate shuttle across the inner mitochondrial membrane. Disruption of the shuttle is associated with impaired energy production in the mitochondria, which reduces the metabolic activity of ILC2 immune cells in adipose tissue.
"Taken together, our findings describe a self-reinforcing mechanism by which elevated levels of free fatty acids in obesity disrupt ILC2 metabolism and, consequently, the self-regulation of adipose tissue," says co-first author Maria Rafailia Theodorou, formerly a doctoral student in Wilhelm's research group.
Inhibition of ACC1 disrupts the activity of ILC2 immune cells
Through its research, the Bonn team linked the underlying causes of metaflammation to potential changes in immune cell metabolism. Certain side effects observed in the treatment of obesity and diabetes could be attributed to adverse effects on that metabolism.
"Thus, targeting of adipose tissue metabolism may fail without appropriate consideration of the effects on the immune system," says Wilhelm, who is a member of the Cluster of Excellence ImmunoSensation3 and the Transdisciplinary Research Area (TRA) "Life and Health" at the University of Bonn. "A more comprehensive approach that considers immune cell metabolism could inform the development of more effective therapies in this area."
Publication details
Fotios Karagiannis et al, Adipose ILC2s depend on acetyl-CoA carboxylase 1 to maintain metabolic health, Cell Metabolism (2026). DOI: 10.1016/j.cmet.2026.08.019
Journal information: Cell Metabolism
Key medical concepts
Clinical categories
Allergy and immunologyEndocrinologyWeight management Provided by University Hospital of Bonn Who's behind this story?
Gaby Clark
MA in English, copy editor since 2021 with experience in higher education and health content. Dedicated to trustworthy science news. Full profile →
Andrew Zinin
Master's in physics with research experience. Long-time science news enthusiast. Plays key role in Science X's editorial success. Full profile →
Citation: High-fat diets suppress enzyme in immune cells, promoting fat tissue inflammation in mice (2026, September 23) retrieved 23 September 2026 from https://medicalxpress.com/news/2026-09-high-fat-diets-suppress-enzyme.html This document is subject to copyright. Apart from any fair dealing for the purpose of private study or research, no part may be reproduced without the written permission. The content is provided for information purposes only.