At the end of September, scientists from University of Virginia revealed the discovery of a total of 17 genes directly involved in the development of obesity. This is an important breakthrough as the COVID-19 pandemic has only worsened this persistent and often overlooked crisis.
It’s no secret that the prevalence rates of obesity in children and adults have steadily increased over the past two decades. In a recent media statement, the Centers for Disease Control and Prevention reported that the number of states in which 35% or more of the population suffered from obesity almost doubled, from nine in 2018 to 16 in 2020. Further analysis of the literature on patients with COVID-19 has revealed as children Pain of obesity had greater disease severity and higher hospitalization rates.
As this invisible epidemic continues to rage in the shadow of COVID-19[feminine, Dr Eyleen O’Rourke, Ph.D. et son Ã©quipe ont travaillÃ© pour comprendre les facteurs gÃ©nÃ©tiques derriÃ¨re l’obÃ©sitÃ©.
Â« Nous connaissons des centaines de variantes gÃ©nÃ©tiques qui sont plus susceptibles d’apparaÃ®tre chez les personnes souffrant d’obÃ©sitÃ© et d’autres maladies. Mais Â«Â plus susceptible d’apparaÃ®treÂ Â» ne signifie pas provoquer la maladieÂ Â» mentionnÃ© O’Rourke, professeur adjoint de biologie et de biologie cellulaire au dÃ©partement de biologie cellulaire de l’UVA School of Medicine et au centre de recherche cardiovasculaire Robert M. Berne. “Nous prÃ©voyons que notre approche et les nouveaux gÃ¨nes que nous avons dÃ©couverts accÃ©lÃ©reront le dÃ©veloppement de traitements pour rÃ©duire le fardeau de l’obÃ©sitÃ©.”
Alors que l’Ã©quipe de recherche Ã©tait en grande partie composÃ©e de membres de l’UVA, des membres supplÃ©mentaires reprÃ©sentaient l’universitÃ© suÃ©doise d’Uppsala, le Broad Institute du MIT et Harvard. Ensemble, les chercheurs ont pu passer au peigne fin des centaines de gÃ¨nes connus pour Ãªtre associÃ©s Ã l’obÃ©sitÃ© et en identifier quelques-uns aux implications prometteuses.
Â«Â Des thÃ©rapies anti-obÃ©sitÃ© sont nÃ©cessaires de toute urgence pour rÃ©duire le fardeau de l’obÃ©sitÃ© chez les patients et le systÃ¨me de santÃ©Â Â», O’Rourke dÃ©clarÃ© dans le communiquÃ© de presse. “Notre combinaison de gÃ©nomique humaine et de tests de causalitÃ© sur des animaux modÃ¨les promet de produire des cibles anti-obÃ©sitÃ© plus susceptibles de rÃ©ussir dans les essais cliniques en raison de leur efficacitÃ© accrue attendue et de leurs effets secondaires rÃ©duits.”
IntriguÃ©, BioSpace s’est entretenu avec O’Rourke dans le but d’en savoir plus sur les rÃ©sultats.
Faire la lumiÃ¨re sur l’invisible
En dÃ©veloppant un modÃ¨le d’obÃ©sitÃ© pour le ver souvent Ã©tudiÃ© C. elegans, avec qui nous partageons une similitude gÃ©nÃ©tique de 70Â % et une rÃ©ponse de gain de poids comparable Ã une consommation excessive de sucre, O’Rourke et son Ã©quipe ont examinÃ© 293 gÃ¨nes soupÃ§onnÃ©s de commettre des crimes cellulaires causant l’obÃ©sitÃ©.
Parmi ceux-ci, un total de 17 gÃ¨nes sont formellement accusÃ©s : ceux qui sont impliquÃ©s dans la causalitÃ© de l’obÃ©sitÃ© sont au nombre de 14, tandis que trois se sont avÃ©rÃ©s capables de jouer un rÃ´le prÃ©ventif.
O’Rouke a notÃ© que l’obÃ©sitÃ© est une maladie complexe et que les progrÃ¨s vers des rÃ©ponses mÃ©canistes dÃ©finitives sont lents. “MÃªme lorsque nous obtenons des rÃ©ponses vraiment prÃ©cises, ces rÃ©ponses sont limitÃ©es Ã ce contexte particulier”, a-t-elle dÃ©clarÃ© Ã BioSpace, prÃ©cisant que l’activitÃ© de ces gÃ¨nes pourrait changer si C. elegans ont Ã©tÃ© nourris avec un rÃ©gime diffÃ©rent, sans haute teneur en fructose. Â«Â Maintenant, ce gÃ¨ne [may not be] do something. Not surprisingly, we have found many cases in which it does the opposite: instead of reducing fat levels, it increases current levels if I change the diet in a different way.
However, as the genes screened were already associated with obesity, the results are still promising. Even better, blocking the activity of a specific preventive gene appeared to improve neurolomotor function and increase the longevity of patients. C. elegans, two traits that are negatively influenced by obesity in humans.
That seems to be enough hope to fuel O’Rourke’s drive to uncover more pieces of the human body’s metabolic puzzle. In the meantime, she encourages more extensive research, saying, âIt is important to remain open-minded about the value of inferior model systems, as well as newer systems, because who says flies, or mice, Where C. elegans offers us the best approximation of human physiology? “I’m sure there are a lot of things in nature that could be very informative that we just aren’t looking at.”
Obesity: the invisible epidemic
Since the Office of the Surgeon General issued a Call to action in 2001, obesity was a recurring topic of discussion. But lack of publicity isn’t the cause of obesity: in fact, the exact causes of obesity are many and varied, ranging from available diet options to fitness choices and individual heredity.
This complexity is why, despite Michele Obama’s school health initiatives from 2008 to 2016 and the many âhealthyâ options on food service menus, childhood obesity rates continue to rise. ascend. Results of the 2017-2018 National Health and Nutrition Survey show that about 16.1% of children in the United States between the ages of 2 and 19 were overweight and 19.3% of them were obese, which includes the 6.1% with severe obesity. A Related A survey carried out during the same period assessed obesity rates among adults and found that the prevalence of adults with the disease was 42.4%.
If only the male stopped the. Unfortunately, childhood obesity is likely to turn into obesity in adulthood, which in turn increases the risk of heart disease, type 2 diabetes, and even some cancers. In total, obesity costs patients and insurers more than 147 billion dollars one year. This represents an average of $ 1,429 more in medical costs for every adult suffering from obesity.
Genetics: the invisible brain
It is commonly believed that obese patients have no one to blame, and this opinion permeates our society from fashion magazines to emergency rooms, even in the most well-intentioned cases. However, the complex pathways between the interconnected systems that govern the body’s fat storage are not yet fully understood.
Research has shown that certain environmental factors are undoubtedly at play: social class, education, ethnicity and gender can all affect a given person’s access to food, as well as the nutritional value of that food. . In addition, studies show that a certain level of stress can cause the body to modify certain epigenetic markers and that some of them modifications maybe both bound obesity as well as transgenerational heritage.
In short, this means that obesity is not only less voluntary than often portrayed in commercial media, but it could also be heavily influenced by a number of inherited variables. Even more gloomy, the right mix of stress and poor nutrition could introduce these genetic variables into a family’s medical history “spontaneously” – meaning researchers and health professionals could observe the equivalent of genetic changes. one-offs that could suddenly appear in millions of current and future Americans, without any traceable origin.
It’s a sobering thought that requires more study and breakthrough like this.