Clinical

14 genes that cause obesity

There’s good news in the fight against obesity-related diseases: There are 14 genes that may promote weight gain, and only three that can prevent it, according to research conducted by the University of Virginia. Treatments for a health issue that affects more than 40% of American adults may now be developed based on the results. “There are hundreds of gene variations that are more prevalent in people with obesity and other illnesses, according to research. It does not imply, however, that it will cause the illness to appear more often. Until we know more about the genetics of obesity, we can’t use population genomics to find new ways to treat or cure it. To get over this obstacle, we created a pipeline that could screen hundreds of genes at once for a connection to obesity. Our first research identified more than a dozen obesity-causing genes and three obesity-preventing genes “according to UVA’s Eyleen O’Rourke, a professor in the Department of Cell Biology at the School of Medicine and the Robert M. Berne Cardiovascular Research Center’s director. Treatments for obesity will be developed faster using our methodology and newly discovered genes, we expect.

Recent work by O’Rourke sheds insight on how obesity, nutrition, and genetics are all connected. Obesity has spread like wildfire, thanks in large part to sugar and high-fructose corn syrup-laden diets. Sedentary lifestyles are also a significant factor. We do not have complete control over how much fat we store or how efficiently our systems burn meals for energy. If we can find the genes responsible for fat storage, we may be able to stop people from overeating by blocking their activity with medicines. Hundreds of genes have been shown to be linked to obesity by genomicists, indicating that fat people are more likely to have these genes than lean individuals. Determining which genes are directly responsible for promoting or helping to avoid weight gain is proving to be a difficult task. O’Rourke and her colleagues used C. elegans worms to separate wheat from chaff. Their preferred habitat is decaying plants, where they feed on microorganisms. More than 70% of their genes are identical to those of humans. They also develop obesity when given an excessive quantity of sugar.

The worms have benefited science greatly. They’ve helped scientists figure out how popular medications like Prozac (a antidepressant) and metformin (a glycemic stabilizer) operate. Three Nobel prizes have been given out in the past 20 years for the discovery of cellular processes initially seen in worms but later shown to be important in illnesses such as cancer and neurodegeneration. This is even more remarkable.. They’ve also proven important in the creation of RNA-based medicines. O’Rourke and her colleagues employed worms to screen 293 human obesity-related genes to determine whether genes were really responsible for or prevented obesity, according to new research published in the scientific journal PLOS Genetics. Using a worm model of obesity, they fed some worms a normal diet while others were fed high-fructose corn syrup.

They were able to discover 14 obesity-causing genes and three obesity-prevention genes using this obesity model in conjunction with automation and supervised machine learning-assisted testing. A fascinating discovery was made by researchers who discovered that by preventing obesity-causing gene activity, the worms were able to live longer and perform better neurologically. Anti-obesity medications have the potential to provide these kinds of advantages to pharma companies. Of course, more work has to be done. However, the results of the study show that the indications are positive. Lab mice that had their weight gain stopped, insulin sensitivity was enhanced, and blood sugar levels were decreased as a result of a gene that was blocked in the study. Furthermore, since the genes under investigation were shown to be linked with obesity in humans, the findings suggest that they will hold true in humans as well, the researchers said. To lessen the cost of obesity on individuals and the healthcare system, O’Rourke stated, “anti-obesity treatments are urgently required.” As a result of the combination of human genomes and causality testing in model animals, we expect that our anti-obesity targets will be more effective and have fewer adverse effects in clinical trials.

Journal Reference: Wenfan Ke, Jordan N. Reed, Chenyu Yang, Noel Higgason, Leila Rayyan, Carolina Wählby, Anne E. Carpenter, Mete Civelek, Eyleen J. O’Rourke. Genes in human obesity loci are causal obesity genes in C. elegansPLOS Genetics, 2021; 17 (9): e1009736 DOI: 10.1371/journal.pgen.1009736

Categories: Clinical