Removing damaged and dysfunctional fat cells from the body could help improve the symptoms of Type 2 diabetes, suggests research from the University of Connecticut.
The study, published in the journal Cell Metabolism, showed that clearing these ‘senescent’ cells using experimental drugs at least once a month reduced symptoms and slowed down 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 system due to the range of long-term health problems that individuals who develop it go on to experience.
“Obesity accelerates the aging processes and is among the most significant risk factors for the development of type 2 diabetes, one of the leading causes of death for older adults,” write the researchers.
Insulin resistance is responsible for many cases of type 2 diabetes. It is caused by a variety of well-known factors including obesity, plus lack of exercise and a poor diet. However, 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 transition from a ‘prediabetic’ back to a normal metabolic state under certain conditions. But such strategies are fairly limited and more information is needed to help slow and even reverse more cases of type 2 diabetes.
Ming Xu, assistant professor in the UConn Center on Aging and the department of Genetics and Genome Sciences at UConn Health, led the current study to investigate the role of senescent cells in diabetes and insulin resistance.
By studying tissue 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 senescence.
The team then created a mouse model expressing p21. They found that senescent cells expressing high levels of p21 could be cleared using the drug dasatinib, currently approved to treat certain types of leukemia, plus quercetin, an antioxidant currently under investigation for various medical indications. This drug combination cleared cells high in p21 in human tissue and reduced symptoms of insulin resistance in the model mice. Xu and colleagues found that clearing these cells once a month effectively slowed type 2 diabetes development and reduced symptoms in these mice.
“These drugs can make human fat healthy, and that could be great,” commented Xu in a press statement. “The results were very impressive and cleared the route for potential clinical trials.”
The team emphasize that while these results are very promising, the research is at an early stage and needs to be confirmed in further studies in both animals and humans. “Large scale clinical trials are absolutely critical to examine the efficacy and safety of these drugs in humans before clinical use,” said Xu.
