The senescent cells or dysfunctional found in human fat, once eliminated, relieve the symptoms of type 2 diabetes such as insulin resistance and a tendency to obesity. To declare it are the researchers of UConn Health. The discovery could lead to new treatments for type 2 diabetes and other metabolic diseases.
Currently the country with the highest level of obesity in Europe, with more than 1 adult on 4 (28.1%) obese and almost two out of three (63.4%) overweight is England. Over the next 20 years, the number of obese adults in the country is projected to rise to 26 million.
According to experts, such an increase would result in more than a million more cases of type 2 diabetes, heart disease and cancer. Obesity is no longer a condition that only affects older people, although the likelihood increases with age and an increasing number of young people have been diagnosed with obesity.
The cells of our body are constantly renewing themselves: cells that age and die and new ones are born. But sometimes this process goes wrong. Damaged cells occasionally persist.
Called senescent cells, they hang around, acting as a bad influence on other nearby cells. Their bad influence changes the way neighboring cells handle sugars or proteins and thus cause metabolic problems.
The results of the Research have been published in the scientific journal Cell Metabolism.
Senescent cells: this is why it is important that they are eliminated
Type 2 diabetes is the most common metabolic disease in the United States. According to the Centers for Disease Control and Prevention (CDC), about 34 million people suffer from it, or one for every 10 inhabitants of the United States.
Most people with diabetes have insulin resistance, which is associated with obesity, lack of exercise, and poor nutrition. But it also has a lot to do with the senescent cells in people’s body fat, according to the new findings Ming Xu and colleagues of the UConn Health School of Medicine.
The elimination of senescent cells appears to stop the typical symptoms of type 2 diabetes in obese mice. Ming Xu, assistant professor at the UConn Center on Aging and the Department of Genetics and Genome Sciences at UConn Health, led the research, along with researchers from UConn Health Lichao Wang And Binsheng Wang as main contributors.
Relieving the negative effects of fat on metabolism was a major achievement, the researchers stated. If a therapy worked so well in humans, it would be a revolutionary treatment for diabetes.
Xu and his colleagues tested the effectiveness of a combination of experimental drugs, dasatinib And quercetin. Dasatinib and quercetin had already been shown to prolong life span and good health in aged mice.
In this study, they found that these drugs can kill senescent cells from human fat tissue cultures. The tissue was donated by obese individuals known to have metabolic problems. Without treatment, human fatty tissues induced metabolic problems in the immunodeficient mice. After treatment with dasatinib and quercetin, the damaging effects of adipose tissue were almost eliminated.
“These drugs can make human fat healthy, and that could be great,” says Xu. “THE the results were very impressive and paved the way for potential clinical trials ”.
Xu and his colleagues at UConn Health and the Mayo Clinic are now using the combination of dasatinib and quercetin in clinical trials to see if the drugs can improve type 2 diabetes in human patients.
“While these preclinical results were very promising, large-scale clinical trials are absolutely critical for examining the efficacy and safety of these drugs in humans prior to clinical use.“Xu pointed out.
The research team is also focusing on a previously unexplored population of senescent cells. These senescent cells express high levels of p21, a cyclin-dependent kinase inhibitor and one of the key markers for cellular senescence.
Using a newly developed mouse model, Xu’s team demonstrated that eliminating these senescent cells once a month is effective in both slowing the development of diabetes and relieving the diabetic symptoms developed in obese mice.
Xu explained that previous research has focused on several cell markers, but that the effects of clearing highly p21-expressing cells have been so marked in relieving diabetes that this marker should receive more attention.
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