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Key protein discovered to combat obesity

Key protein discovered to combat obesity

A research project from the University of Barcelona (UB), in Spain, allowed the identification of a protein —the ACBP— which can help improve control of obesity and cardiovascular disease.

The research was published in the journal Molecular Metabolism and was led by Professor Francesc Villarroya of the Faculty of Biology and the Institute of Biomedicine at the UB. The Sant Joan de Déu Research Institute (IRSJD) and the Obesity Pathophysiology Department of the University of Barcelona (CIBEROBN) also participated in the study.

Obesity, diabetes, and cardiovascular disease are increasingly prevalent in the population, and brown adipose tissue is known to play a protective role against these prevalent diseases, as it burns calories and is capable of producing body heat from fat.

But as the body ages, brown adipose tissue activity declines, and this deactivation of brown adipose tissue function—typical of obese individuals—has not yet been widely studied in the scientific literature.

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The UB research discovered for the first time a molecule that represses the activity of brown adipose tissue, and the work opens new avenues for understanding why and how the inactivation of this key tissue for metabolizing fats in the body occurs. This could be very useful for determining whether this repressive function can be reversed and help design strategies for the treatment of obesity and cardiometabolic diseases.

There are two types of adipose tissue in the body: white adipose tissue—the energy reserve in the form of lipids—and brown adipose tissue—the main heat-generating organ in the body through thermogenesis.

According to Francesc Vilarroya, "the problem is knowing what causes brown fat activity to decrease," and until now, "it was generally assumed that the low activity of brown fat in aging and obesity could be explained by its activators not working properly."

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The new research, conducted using animal models, describes a repressor factor that blocks brown fat activity: the ACBP protein. Under normal conditions, this protein would intervene when brown fat activity is not needed, for example, in a warm environment.

However, the aforementioned protein is also implicated in aging and in the pathological blockage of brown adipose tissue that promotes obesity.

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The ACBP protein's regulatory activity reveals other biomedical implications in the fight against diseases such as cancer.

According to Vilarroya, "in some types of cancer, brown adipose tissue becomes pathologically overactivated, causing uncontrolled metabolic energy expenditure that leads to cachexia—extreme malnutrition and muscle atrophy."

In this case, the function of the ACBP protein as a repressor factor could become an interesting therapeutic tool for cancer patients, Villarroya explains.

In another context, it is also known that global warming caused by climate change promotes obesity, since an increasingly warm environment leads to inactive brown adipose tissue.

"An excess of the ACBP protein, which blocks the activity of brown fat, could be the molecular basis for this phenomenon," Vilarroya explains.

Once this factor is identified, "we can design intervention tools to promote a healthier lifestyle," this researcher concludes.

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