Brett Smith for redOrbit.com – Your Universe Online
Managing Type 2 diabetes may include the need for daily medications or regular insulin injections, but a new study indicates that a protein called FGF1 could be the key to longer-lasting, more effective medications.
[ Watch the Video: Discovery Of Molecule’s Role May Lead To A Diabetes Cure ]
Published in the journal Nature, the new study discovered that treatment together with the protein doesn’t merely maintain blood sugar, but it also removes insulin insensitivity, the underlying biological cause of all forms of diabetes. The researchers added that the recently developed treatment method doesn’t lead to side effects typical to most current diabetes remedies.
“Controlling glucose is a dominant problem in our society,” said study author Ronald M. Evans, director of Salk Institute’s Gene Expression Laboratory, in a recent statement. “And FGF1 offers a new method to control glucose in a powerful and unexpected way.”
A condition that affects nearly 30 million Americans, Type 2 diabetes occurs when glucose increases in the circulatory system due to inadequate sugar-transporting insulin being made or due to the fact cells are getting to be insulin-resistant, disregarding signals to take in sugar. Being a chronic condition, diabetes might cause substantial health issues and has no cure. However, it can be managed through a blend of diet, regular exercise and medications.
Medications currently on the market try to boost levels of insulin and turn back insulin resistance by shifting expression of genes aimed at lessening glucose levels within the blood. However, some drugs boost the body’s generation of insulin to the point that glucose levels drop too low and lead to life-threatening hypoglycemia, and other side effects.
In 2012, Salk researchers noticed that mice without the growth factor FGF1 swiftly developed diabetes when given a high-fat diet, a finding which indicated FGF1 played a major role in controlling blood glucose levels. This led the scientists to consider if supplying extra FGF1 to diabetic mice could treat symptoms of the condition.
To test their theory, the scientists injected FGF1 into overweight mice with diabetes to gauge the protein’s prospective influence on metabolism. Scientists discovered that with a single dose, blood sugar levels rapidly dropped to normal levels in all the test subjects.
“Many previous studies that injected FGF1 showed no effect on healthy mice,” said study author Michael Downes, a senior staff scientist at Salk. “However, when we injected it into a diabetic mouse, we saw a dramatic improvement in glucose.”
The study revealed FGF1, even at large doses, did not cause side effects observed with traditional medications or cause blood sugar levels to drop to dangerously lower levels, a risk associated with numerous of glucose-lowering substances. Instead, the injections reconditioned the body’s own capacity to naturally normalize insulin and blood sugar levels, maintaining glucose amounts within a secure range. Essentially, FGF1 reversed the key symptoms of diabetes.
“With FGF1, we really haven’t seen hypoglycemia or other common side effects,” said Jae Myoung Suh, a co-author of the study and postdoctoral research fellow at Salk. “It may be that FGF1 leads to a more ‘normal’ type of response compared to other drugs because it metabolizes quickly in the body and targets certain cell types.”
The study team said they weren’t able to describe the exact mechanism behind the effects of FGF1 but said their work is the first step in using the protein to develop a therapeutic drug.
“We want to move this to people by developing a new generation of FGF1 variants that solely affect glucose and not cell growth,” Evans said. “If we can find the perfect variation, I think we will have on our hands a very new, very effective tool for glucose control.”