New findings on how adipose tissue influences intestinal inflammation

How adipose tissue shapes intestinal inflammation

 

Researchers at Charité – Universitätsmedizin Berlin and the Max Delbrück Center for Molecular Medicine have gained new insights into the role of adipose tissue in chronic intestinal inflammation as part of the new ImmunoPreCept Cluster of Excellence.

What was the research question or scientific inquiry behind your study?

Chronic gut inflammation arises when the balance between the intestinal barrier, gut microbes, and the immune system is disturbed. We wanted to find out whether signals from fat tissue play an active role in this process. Specifically, we studied whether substances released by fat tissue, like leptin, can activate immune cells, trigger inflammation in the gut, and weaken the intestinal barrier.

How did you approach the study?

We studied mice without fat tissue and a patient with acquired generalized lipodystrophy (AGLCD), a rare disorder causing complete loss of body fat. In the mice, we looked at inflammation, gut barrier function, and how transplanting fat tissue affected these. In the patient, we examined immune cells and the effects of treatment with leptin.

What did you discover?

Mice without fat tissue were surprisingly protected from gut inflammation and had a stronger intestinal barrier. When fat tissue was transplanted back, inflammation returned, but only if the tissue could produce leptin. Fat tissue that could not make leptin had no effect. Interestingly, the patient with AGLCD developed Crohn’s disease even without any fat tissue.

Was there anything that surprised you?

We were surprised that the patient developed chronic gut inflammation despite having no fat tissue and no natural leptin, which at first seemed to contradict our mouse results. However, detailed genetic analyses showed that the patient’s immune cells had an acquired mutation that promotes inflammation. When treated with leptin, the number of inflammation-promoting immune cells increased even more.

What’s your takeaway?

Our findings show that fat tissue actively regulates immune responses of the gut. Signals released from fat tissue can boost inflammatory reactions in the intestine. At the same time, the patient case demonstrates that acquired genetic changes in immune cells can also drive inflammation, which can be further amplified by strong signal from fat tissue, like leptin. Fat tissue is not just an energy store; it also helps regulate the immune system and protect the gut. This may explain why severe obesity can raise the risk of chronic inflammatory bowel diseases like Crohn’s disease. For daily life, it shows that metabolism, inflammation, and gut health are closely linked. In the long run, these insights could help develop more personalized treatments.


More information:


Contact

Prof. Carl Weidinger & Prof. Britta Siegmund
Department of Gastroenterology, Infectious Diseases and Rheumatology (including Clinical Nutrition)
Campus Benjamin Franklin
Charité – Universitätsmedizin Berlin

 

     

     

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