Removing damaged and dysfunctional fat cells from the body can help improve the symptoms of type 2 diabetes, research from the University of Connecticut suggests.
The study, published in the journal Cell metabolism, showed that clearing these ‘aging’ cells using experimental drugs at least once a month reduced symptoms and slowed the development of diabetes in a mouse model.
Type 2 diabetes affects a large number of people, up to 1 in 10 Americans, and has a huge impact on the health care system due to the range of long-term health problems that people who develop it continue to experience.
“Obesity accelerates the aging process and is among the major risk factors for developing type 2 diabetes, one of the leading causes of death for older adults,” the researchers write.
Insulin resistance is responsible for many cases of type 2 diabetes. It is caused by a number of well-known factors including obesity, plus lack of exercise and a poor diet. But other things also contribute to this, including senescent fat cells.
While insulin resistance often leads to type 2 diabetes, it is not inevitable and people can, under certain conditions, switch from a ‘pre-diabetic’ back to a normal metabolic state. However, such strategies are quite limited, and more information is needed to help curb and even reverse more cases of type 2 diabetes.
Ming Xu, assistant professor at the UConn Center for Aging and the Department of Genetics and Genomics at UConn Health, led the current study to investigate the role of aging cells in diabetes and insulin resistance.
By studying tissues donated by obese individuals with insulin resistance, the researchers found a small population of fat cells that express high levels of a chemical known as p21, a cyclin-dependent kinase inhibitor, which is a marker of cell dysfunction and old age.
The team then created a mouse model expressing p21. They found that aging cells expressing high levels of p21 could be purified using the drug dasatinib, which is currently approved for the treatment of certain types of leukemia, plus quercetin, an antioxidant currently under study for various medical indications. This drug combination removed cells with high p21 content in human tissue and reduced symptoms of insulin resistance in model mice. Xu and colleagues found that clearing these cells once a month effectively slowed the development of type 2 diabetes and reduced symptoms in these mice.
“These drugs can make human fat healthy, and it could be amazing,” Xu commented in a press release. “The results were very impressive and paved the way for potential clinical trials.”
The team stresses that although these results are very promising, the research is at an early stage and needs to be confirmed in further studies on both animals and humans. “Large-scale clinical trials are absolutely essential to study the efficacy and safety of these drugs in humans before clinical use,” Xu said.
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