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Fat accumulation in immune cells not the source of chronic inflammation after all

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March 4, 2020

Metabolic diseases such as diabetes may be caused by chronic inflammation in the body. Until recently it was thought that fat accumulations in immune cells caused this inflammation but Wageningen University & Research has now shown that these immune cells continue to stimulate inflammation even when they lose their fat.

Obesity often results in a low-grade but chronic inflammation. Various studies show that this type of inflammation could cause metabolic diseases such as diabetes and cardiovascular disorders. Diets affect the level of inflammation; what people eat or drink can accelerate or slow down the inflammation.

Fatty immune cells

It was commonly thought that this light but chronic inflammation was caused by ‘fatty’ immune cells called macrophages. Macrophages are white blood cells that play an important role in the immune system. They consume and digest pathogens, damaged cells and foreign substances. This important function means that macrophages are found throughout the human body. When someone’s weight increases and their fat tissue expands, macrophages will ‘eat’ the excess fat. The fat is then stored in droplets inside the cells. For many years, scientists thought that fat accumulation prevent the macrophages in the fat tissue from working properly, resulting in a low-grade, chronic inflammation in the body.

Normal macrophage with fat accumulation. The fat droplets are fluorescent colored and the photo was taken with a confocal laser microscope. (Photo: Montserrat de la Rosa)
Normal macrophage with fat accumulation. The fat droplets are fluorescent colored and the photo was taken with a confocal laser microscope. (Photo: Montserrat de la Rosa)
Macrophage without HILPDA, the macrophage no longer stores fat in the droplets. (Photo: Montserrat de la Rosa)
Macrophage without HILPDA, the macrophage no longer stores fat in the droplets. (Photo: Montserrat de la Rosa)

Light chronic inflammation

Scientists from Wageningen University & Research have studied the role of HILPDA, a protein that appears to stimulate fat accumulation in macrophages. Research using mice showed that the fat accumulation in macrophages is not the trigger that causes inflammation. They found that the fats in macrophages were broken down when HILPDA was removed and the fat immune cells became ‘lean’ again. Contrary to what was expected based on the current insights, these lean macrophages still caused a low-grade chronic inflammation and insulin resistance. The results were published in the journal Cell Reports.

Understanding diseases

Xanthe van Dierendonck, lead author of the publication and scientist at the Human Nutrition & Health department of Wageningen University & Research, explains the importance of the study: “To understand diseases like atherosclerosis, fatty liver or diabetes, it is crucial to find out how immune cells behave during these illnesses and how they cause the low-grade chronic inflammation. Our results show that we may be on the wrong path when looking at fat accumulation in macrophages and should expand our scope in future research to gain insight into this inflammatory process.”