FGF1 Protein May Help in Treating Diabetes More Effectively

Present drugs for controlling blood sugar in type 2 diabetes – which takes place when the body turns into desensitized to insulin – come with the danger that blood-sugar levels fall too low. Now in a research of mice with the equivalent of type-2 diabetes, scientists were stunned to discover just one injection of the growth factor FGF1 decreased blood sugar to regular levels without any side effects for more than 2 days.

One dose of FGF1 protein leads to drop of blood glucose to normal level in mice for more than 2 days.

Reporting in the journal┬áNature, the scientists – lead by a team from the Salk Institute for Biological Studies – say they think their results will guide to a new generation of better and more effective medication for diabetes.

As all we know there are 2 types of diabetes type 1 and type 2. Rates of type 2 diabetes have increased in the last 20 years, to the point where reports propose around 30 million People in America have the type 2 diabetes.

As a long-term disease, type 2 diabetes can cause serious health issues. There is no heal till now, alternatively the disease is controlled with different levels of success via drugs and lifestyle adjustments, such as diet, weight reduction and regular physical exercise.

Treating diabetic mice with FGF1 inverted insulin resistance

What amazed the scientists in this new research was that treating the mice with FGF1 – fibroblast growth factor 1 protein – did not only maintain glucose in control, but also inverted insulin resistance. As well as, there were no side-effects that generally come with present available ┬ádiabetes therapies.

Corresponding author Ronald M. Evans states that:

“Managing glucose is a major issue in our society. And FGF1 provides a new method to manage glucose in a highly effective and unexpected way.”

Present medicines for diabetes try to decrease blood glucose by modifying gene expression to increase insulin levels and invert insulin resistance. One model is Byetta, which raises insulin production. But often this can consequence in glucose dropping too far, which leads to life-harmful hypoglycemia, and other unwanted side effects.

In 2012, Prof. Evans and co-workers presented making an unexpected finding: mice inadequate FGF1 easily develop diabetes when given a high-fat diet. They recommended this meant the protein was significant for managing glucose levels.

That outcome lead the group to wonder whether providing the growth factor to diabetic mice may affect the symptoms of the condition.

After giving a single dose, blood glucose decreased to regular levels, with no Adverse effects. The scientists proceeded by giving doses of FGF1 into overweight mice with diet-caused diabetes – a mouse model that is usually used as the similar of type 2 diabetes in human beings. They were surprised by the powerful effect that the protein had on the mice’s metabolism: after sing dose of FGF1 blood glucose levels dropped to normal levels in all treated mice and remained there for more than 2 days.

Present diabetic medication leads to danger of glucose decreasing to dangerous levels which cause undesirable side effects like as weight gain and heart and liver issues.

But the group identified that even at higher doses, FGF1 did not leads to these side effects in the mice. By activating the body’s natural capability to control insulin, the protein maintained blood glucose in a normal level – successfully preventing the number one symptom of diabetes.

The scientists think among the factors why FGF1 has a more “normal” response are that it focuses on particular cell types and metabolizes rapidly.

However, they admit they do not fully recognize how FGF1 functions – just as there still many un-answered concerns around insulin resistance itself.

Team is planning for clinical trials, but still long way to go

But the scientists say they did discover the protein’s capability to activate growth is completely separate from its effect on glucose, something that is essential to know when considering it as a drug candidate.

Prof. Evans states that he and his co-workers now want to discover out which signaling paths are engaged when FGF1 acts on glucose to affect diabetes and metabolism.

They are currently planning clinical trials, but say it will take time to fine-tune the protein into a medicine for therapeutic use.

“We wish to move this to individuals by developing a new generation of FGF1 variants that completely affect glucose and not cell growth,” states Prof. Evans. “If we can discover the perfect variation, I think we will have a very novel, very successful tool for glucose control.”