Researchers in the US have found that targeting old or senescent cells in the fat tissue of obese mice can alleviate diabetes – a result they hope could lead to new ways to treat the condition in people.
The findings by University of Connecticut scientists may be of particular interest in the UAE given the high frequency of diabetes in the population.
Almost one in five of the population in the Emirates has the condition, which can lead to serious complications involving the heart, eyes and kidneys.
In their study, the scientists looked at the role that senescent or “zombie” cells play in Type 2 diabetes, the form associated with lifestyle factors such as being overweight or inactive.
With Type 2 diabetes, the level of glucose in the blood can become too high because of insulin resistance, where cells in the body do not respond as they should to the hormone insulin.
Senescent cells in body fat may play a role in this, because the study found that clearing them out could combat diabetes in the mice, achieving what the university described as “a dramatic result”.
Published in the journal Cell Metabolism, the study reported that two drugs, dasatinib and quercetin, could kill senescent cells from human fat tissue grown in the laboratory.
Also, when the human fat cells were transplanted into mice, they caused diabetes in the creatures but the same two drugs could stop this.
“These drugs can make human fat healthy and that could be great,” Dr Ming Xu, an assistant professor involved in the work, said in a statement.
“The results were very impressive and cleared the route for potential clinical trials.”
The university researchers and their co-authors from a medical centre, the Mayo Clinic, aim to hold clinical trials to see if the two drugs can alleviate Type 2 diabetes in people.
“Although these preclinical results were very promising, large-scale clinical trials are absolutely critical to examine the efficacy and safety of these drugs in humans before clinical use,” said Dr Xu.
A substance called p21, found in high levels in the senescent cells, may be important in the processes the scientists studied. When the researchers removed cells expressing high levels of p21 each month from obese mice, diabetes was alleviated.
Finbarr O’Harte, a professor of endocrinology and metabolism at Ulster University in Northern Ireland, who is not connected to the study, said the research “certainly seems like an interesting prospect”.
“In diabetes and obesity you have long-term inflammatory disorders in the fat tissue,” he said.
“This may be one way of remedying this inflammatory disorder and rectifying diabetes. It’s an interesting idea.”
He said that mice have been “used widely” as models for diabetes although it is uncertain if a result with them will translate into people.
“It’s never a given that because it works on a mouse it will work on a human,” he said.