New drug therapy ‘reverses’ diabetes in mice
pharmafile | March 29, 2017 | News story | Research and Development | diabetes
A team of researchers at the University of California, San Diego (UCSD) have developed a drug therapy which has shown to ‘reverse’ the effects of diabetes in mice by restoring the body’s sensitivity to insulin, opening the door for potential new methods to rectify abnormal blood sugar levels.
The therapy is a daily, oral pill which inhibits low molecular weight protein tyrosine phosphatase (LMPTP), an enzyme which contributes towards insulin resistance in cells. This leads to the reactivation of insulin receptors on cell surfaces which absorb excess sugar from the blood in the presence of insulin.
The drug was administered to mice that had been fed a high-fat diet, causing them to develop type 2 diabetes. It did not seem to prompt any adverse reactions in the animals.
Past therapies have focused in the same area, on a similar tyrosine phosphatase enzyme, but have run into difficulties targeting it without causing unwanted side effects. These findings could lead to entirely new ways of approaching diabetes treatment.
“Finding a way to make cells respond to insulin again is an important and exciting strategy,” remarked Diabetes UK’s Emily Burns. “So far, the drug has only been tested in mice, and while some research in human genetics suggests this approach could work in people too, we need more research before we know how relevant this could be for people with type 2 diabetes.”
“Our inhibitor increased activation of the insulin receptor in the liver, and reversed diabetes without any apparent negative side effects,” explained Stephanie Stanford, leader of the team at UCSD. “Our compound is very specific for the target, and we do not see any side effects after treatment in mice for a month, but the next step is to rigorously establish if it’s safe for use in clinical trials,”
The number of people with diabetes in the UK is on the rise, growing by 65% over the last ten years to reach over four million in 2016.
Matt Fellows
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