Brain protein acts on neurons to control body weight

A study led by researchers at the University of Montreal Hospital Research Center (CRCHUM) demonstrated for the first time that acyl-CoA binding proteins or ACBP in mice have a direct effect on neurons, keeping rodents and humans healthy. The findings were published in the Journal of Clinical Research.

With the improvement of living standards and the lack of exercise, irregular work and other reasons, there are more and more obese people. And obesity tends to be younger. Because obesity increases the risk of chronic diseases such as type II diabetes, cardiovascular disease, and certain cancers, the World Health Organization considers obesity to be a global public health problem.

As early as 2015, CRHUM's research team has found that ACBP allows astrocytes to transmit changes in blood fatty acids and blood lipids to neurons. Astrocytes, the most widely distributed cell in the mammalian brain, are also the largest of the glial cells. These glial cells are star-shaped, emitting many long and branched protrusions from the cell body, stretching and filling between the cell bodies of the nerve cells and their processes, supporting and separating nerve cells. Because of the effects of ACBP on astrocytes, the brain can adjust food intake and energy expenditure, and ultimately control the owner's weight.

Together with colleagues at the NutriNeuro laboratory at the University of Bordeaux, the team identified neurons that reduce food intake, called proopiomelanocortin neurons or POMC neurons. POMC neurons communicate closely with astrocytes that produce protein ACBP in specific regions of the brain. This particular area is the arcuate nucleus of the hypothalamus.

The arcuate nucleus of the hypothalamus is essential for controlling feeding and metabolism. When activated, the arcuate nucleus of the hypothalamus contains two sets of neurons with opposite functions: the first group leads to an increase in food intake; the second group of POMC neurons shared by animals and humans promotes a reduction in food intake and increase in energy consumption.

Five percent to ten percent of obesity cases are caused by genetic mutations. A large proportion of these cases are associated with disruption of the neural pathway commonly referred to as the melanocortin pathway. And the researchers observed that the loss of ACBP gene in astrocytes of the arcuate nucleus promotes obesity.

The team used ACBP to inject a genetically modified obese mouse model daily, and after 5 days the mice had a food intake and weight loss of about five percent. This mechanism relies on ACBP to activate POMC neurons.

However, the study is currently in the basic research phase and is only performed in mice in the laboratory. So they believe that applying this discovery to humans requires further research and exploration.