This study, the results of which are published in the journal Science, could lead to the development of new drugs to control appetite.
People suffering from overweight or obesity often say that they have difficulty controlling their appetite: they are hungry all the time. However the feeling of hunger could come from the malfunction of a “satiety switch”, that is to say an enzyme encoded by the genes of cells located in the hypothalamus, according to a new study published in the scientific journal Science. A discovery that could allow the development of more effective treatments against obesity, when we know that 6.5 million French people are affected (including 3.5% of children).
These astonishing results are in fact due to chance. A team of researchers from Johns Hopkins University in the United States originally studied the strength of connections between neurons (in the brains of laboratory mice), which are known to be important for learning and memory. In particular, they wanted to find out what the consequences would be if the gene encoding the OGT enzyme were deliberately deactivated. OGT is known to have a role in several metabolic functions, including the regulation of insulin and blood glucose.
The mass of mice doubles in two weeks
Still, the researchers quickly realized that the mice in which they had blocked the expression of OGT had gained weight. A lot of weight even: the mass of the mice had doubled in two weeks. “These mice did not understand that they had eaten enough, so they continued to feed,” says Olof Lagerlof, researcher at Johns Hopkins University, and first author of the study published in the journal. Science.
Astonished by these results, the scientists set out to find out what would happen if they simulated the opposite effect, forcing the enzyme OGT to be produced.
An enzyme that regulates the effect of satiety
“If you artificially increase the activity of this gene, you can make a hungry mouse stop eating,” says Richard Huganir, research director at Johns Hopkins University. According to the study, mice could eat up to 25% less per day when the activity of the gene in question was artificially increased.
Results of this experiment, the enzyme could “regulate the balance of the effect of satiety”, still declares Richar Huganir. A satiety switch, which if damaged could lead to obesity situations.
“We believe we have discovered a new receptor of information that directly affects brain activity and eating behavior, and if our findings are replicable in other animals, including humans, they could lead to the discovery of new drugs, or new techniques to control appetite, ”suggests Lagerlof.
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