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Immune Cells Show New Ways To Treat Obesity, Insulin Resistance, Type 2 Diabetes And Fatty Liver

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Macrophages are immune system cells that control inflammation and tissue function in addition to being crucial in the early response to microbial infection.

Inflammation is a normal bodily response that helps repair damaged tissue. However, if it isn’t taken care of properly, it can turn into chronic inflammation, which is the root cause of many diseases, such as metabolic syndrome, which is linked to obesity, type 2 diabetes, and heart disease.

Now, a group of researchers at the Centro Nacional de Investigaciones Cardiovasculares (CNIC) has found that macrophages have different metabolic needs depending on which organ they are in. These cells, in other words, adjust to the requirements of the organ in which they are found.

The findings give “us a better understanding of how macrophages regulate their metabolism according to the organ in which they reside,” according to study leader Dr. David Sancho. 

Furthermore, adds the author, these “results reveal a vulnerability of macrophages that contributes to chronic inflammatory diseases and that could be exploited therapeutically for the treatment of conditions associated with obesity and metabolic syndrome, such as cardiovascular disease.”

Immunity released the research today.

Macrophages are immune cells that are generally spread throughout the body and help in the removal of all forms of biological material from organs, including dangerous particles such as mineral crystals or viruses, as well as proteins and bigger complexes that form throughout development.

Immune System Discovery Paves Way for Revolutionary Treatments for Obesity-Related Diseases

Macrophages are crucial for eliminating dead cells, which helps with tissue regeneration. According to the latest research, macrophages modify their metabolism and behavior depending on the organ they are housed in.

“In tissues with abundant extracellular fat and cholesterol, such as the lungs and spleen, macrophages adapt their metabolism to degrade these fats through mitochondrial respiration,” adds first author Dr. Stefanie Wculek. “Using genetic or pharmacological methods to disrupt mitochondrial respiration, mitochondria can be eliminated from lung and spleen, whereas the macrophages in other organs, which don’t depend on mitochondrial respiration, survive.”

The macrophages that live in adipose tissue, or body fat, are another example.

“Macrophages residing in the body fat of a person of normal weight are unaffected by mitochondria-disrupting treatments because their metabolism is less dependent on mitochondrial respiration. This is because the fat cells, called adipocytes, are fully functional, leaving the macrophages in a resting state,” explains Dr. Sancho. “However, in obese individuals, the excess fat surpasses the capacity of the adipocytes, and the resident macrophages become activated, converting into inflammatory cells that promote the development of insulin resistance, type 2 diabetes, and fatty liver.”

But this change in the macrophages of adipose tissue also makes them weak.

According to Dr. Sancho, “the activated macrophages depend on mitochondrial respiration to process the excess fat, and this makes them vulnerable to therapeutic interventions, including pharmacoligical inhibitors of mitochondrial respiration.”

The Immunity research demonstrates that activating mitochondrial respiration destroyed these proinflammatory macrophages, halting the development of obesity, type 2 diabetes, and fatty liver (the main elements of metabolic syndrome) in a model animal.

The researchers came to the conclusion that this finding could lead to new ways to treat diseases like heart disease that are linked to obesity and metabolic syndrome.

Source: 10.1016/j.immuni.2023.01.011

Image Credit: Getty

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