In mice with diet-induced diabetes - the equivalent of type 2 diabetes in humans - a single injection of the protein FGF1 is enough to restore blood sugar levels to a healthy range for more than two days.
The discovery by Salk Institute for Biological Studies scientists could lead to a new generation of safer, more effective diabetes drugs.
The team found that sustained treatment with the protein doesn't merely keep blood sugar under control, but also reverses insulin insensitivity, the underlying physiological cause of diabetes.
"Controlling glucose is a dominant problem in our society. And FGF1 offers a new method to control glucose in a powerful and unexpected way," said Ronald M Evans, director of Salk's Gene Expression Laboratory.
Type 2 diabetes, which can be brought on by excess weight and inactivity, has skyrocketed over the past few decades around the world.
In the disease, glucose builds up in the bloodstream because not enough sugar-carting insulin is produced or because cells have become insulin-resistant, ignoring signals to absorb sugar.
As a chronic disease, diabetes can cause serious health problems and has no specific cure. Rather it is managed through a combination of diet, exercise and pharmaceuticals.
But drugs which increase the body's production of insulin, can cause glucose levels to dip too low and lead to life-threatening hypoglycemia, as well as other side effects.
In 2012, Evans and his colleagues discovered that a long-ignored growth factor had a hidden function: it helps the body respond to insulin.
Unexpectedly, mice lacking the growth factor, called FGF1, quickly develop diabetes when placed on a high-fat diet, a finding suggesting that FGF1 played a key role in managing blood glucose levels.
Evans' team injected doses of FGF1 into obese mice with diabetes to assess the protein's potential impact on metabolism.
Researchers were stunned by what happened: they found that with a single dose, blood sugar levels quickly dropped to normal levels in all the diabetic mice.
The study was published in the journal Nature.
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