The result could be a whole new generation of drugs that could safely and effectively stem the rising type 2 diabetes epidemic.
The magic bullet in this case is the protein FGF1. The Salk experiments discovered that a single injection could restore blood sugar levels to the safe range for several days.
More than just managing the disease
More significant, perhaps, the experiments showed that sustained treatment doesn't just act as a controlling mechanism but actually reduces insulin insensitivity, the underlying cause of the disease.
Type 2 diabetes is different from type 1, in that type 1's cause is mostly genetic while type 2 is largely caused by obesity and an unhealthy lifestyle. Not surprisingly, type 2 is now the more common form of the disease.
When you have diabetes your body causes blood glucose, or sugar levels to rise higher than normal. It's a condition known as hyperglycemia.
When you have type 2 diabetes your body does not use insulin properly, a condition known as insulin resistance. The pancreas tries to compensate for it but over time it isn't able to keep up and can't make enough insulin to keep your blood glucose at normal levels.
No cure – yet
According to the Mayo Clinic there is currently no known cure for type 2 diabetes but the disease can be managed through diet and exercise and maintaining a healthy weight. Medication and insulin therapy helps where lifestyle changes fall short.
No one is using the word “cure” just yet but the Salk scientists say the results of the FGF1 experiments may be a big step in that direction. So far they have found no side effects that might reduce the effectiveness of the treatment or prevent some patients from receiving it.
“Controlling glucose is a dominant problem in our society,” said Ronald Evans, director of Salk's Gene Expression Laboratory and corresponding author of the paper. “And FGF1 offers a new method to control glucose in a powerful and unexpected way.”
The diabetes drugs currently approved for use attempt to boost insulin levels and reverse insulin resistance by altering the expression levels of genes to lower glucose levels in the blood. But the researchers say drugs that increase the body’s insulin production can also cause glucose levels to fall too low and lead to life-threatening hypoglycemia, as well as other side effects.
As many breakthroughs are, this one was something of a surprise. The experiment used obese mice as stand-ins for obese, diabetic humans.
Evans’ team injected doses of FGF1 into the obese mice with diabetes to see how it affected metabolism. Researchers said they 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.
“Many previous studies that injected FGF1 showed no effect on healthy mice,” said Michael Downes, a senior staff scientist and co-corresponding author of the new work. “However, when we injected it into a diabetic mouse, we saw a dramatic improvement in glucose.”
More research is ahead before an FGF1 drug is submitted for FDA approval, but the scientists hope to move next to human trials. Evans says there are still many questions from the study that need to be answered. But, he says, “the avenues for investigating FGF1 in diabetes and metabolism are now wide open.”