Don't crucify yourself for a skipped gym day or a sin of gluttony: weight control could be more of a chemistry problem than you think.
In a study published by the Journal of Clinical Investigation, researchers from the University of Montreal Hospital Research Center (CRCHUM) show for the first time in the world that Acyl-Coenxima A has a direct influence on the neurons that allow rodents and humans to maintain the right weight.
Already four years ago the team, led by Dr. Thierry Alquier, had shown the active role of this protein in allowing astrocytes (the cells that support neuronal functions) to communicate to neurons the changes in fat in the blood. It is thanks to this information that the brain can regulate energy expenditure and needs, effectively controlling weight.
We now know that the neurons responsible for energy needs, known as POMCs, or proopiomelanocortins, are in direct communication with the astrocytes that produce Acyl-Coenxima A in a specific area of the brain: the arcuate nucleus of the hypothalamus.Thierry Alquier, associate professor at the Université de Montréal.
This area, essential for metabolism, is populated by two groups of neurons that have opposite functions: one part of them increases the need, another part reduces it.
"Genetic mutations explain 5 to 10 percent of obesity cases," says Alquier. Among these, a large percentage is linked to an Acyl-Coenzyme A problem: its deficiency leads to obesity, the major risk factor for diabetes, cardiovascular disease and some types of cancer.
Experiments show that administering Acyl-Coenzyme A in obese mice leads to a 5% reduction in weight in five days: it is as if an 80kg man lost 800 grams per day.
As one might expect, the researchers preach caution before they can consider the discovery valid for humans as well: the research is still in a preliminary phase.
Here is the study: Khalil Bouyakdan et al, The gliotransmitter ACBP controls feeding and energy homeostasis via the melanocortin system, Journal of Clinical Investigation (2019). DOI: 10.1172 / JCI123454