JCI Insight: Scientists are expected to develop new therapies for severe obesity

JCI Insight: Scientists are expected to develop new therapies for severe obesity.  In a research report published in the international journal JCI Insight, scientists from the University of Montreal and other institutions may develop treatments for early morbid familial obesity through research. (Early morbid familial obesity) new treatment, this disease affects the health of 4%-6% of people suffering from early obesity.

Researcher Michel Bouvier said that people suffering from this rare disease do not feel full, and satiety is the message that the body transmits to the brain to tell us to stop hunger; the final result is that the patient eats too much, leading to things such as Adverse reactions such as obesity and type 2 diabetes. Using mouse models with modified genomes to reproduce human diseases, researchers have observed the key role of mutations in special genes in the process of body satiety. This gene is called melanocortin type 4 receptor (MC4R, melanocortin). type 4 receptor), when injected with a therapeutic molecule commonly known as a pharmacological chaperone, the researchers observed immediate changes in their behavior in the body of obese mice.

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The researchers said that we are still a long way from developing drugs for use in humans, but the results of the pre-clinical in vivo trials in the early stage are very exciting for us; the incidence of early morbid familial obesity is 1/25 million It is called a rare disease because it is not common in the general population, but the patient is very painful. When a family is struggling with this disease, many family members will often be affected. Because obesity is usually related to the body’s lifestyle habits, and these family members may also be rejected.

Morbid obesity is caused by the ineffectiveness of melanocortin. Melanocortin is a special hormone that can regulate the body’s appetite and energy expenditure. The lack of its receptor will promote the occurrence of obesity, and the melanocortin receptor will make the body black The activity of corticosteroids occurs on the surface of hypothalamic cells in the brain. Researchers have previously discovered that pharmacological chaperone molecules may enable defective receptors to be exported to the cell surface.

Now researchers have discovered that this family of molecules plays a role in human cell lines with different mutations in the MC4R gene. In the article, the researchers describe a new type of mouse model in which the MC4R gene in the body will be mutated normally. The human MC4R gene is replaced; at the same time, the researchers also clarified that a pharmacological chaperone molecule can restore the function of the mutated MC4R gene and significantly reduce the mice’s food intake.

Finally, the researcher Bouvier said that this is not the first time that our laboratory has brought promising pharmaceutical progress to scientists. Under normal circumstances, these rare diseases do not arouse much interest from pharmaceutical companies, because these rare diseases are It is not considered broad enough and not enough to justify a major investment by pharmaceutical companies. Later researchers will continue to conduct in-depth research to find new drugs or therapies to treat this early morbid familial obesity.

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