Researchers at Joslin Diabetes Center have discovered an important cellular process that could be harnessed to diagnose early — and treat — the wide range of complications that stem from diabetes.
Specifically, it linked an RNA molecule to the cellular damage that causes complications in diabetics, and was able to reverse the damage in vitro. The findings, which could help develop biomarkers and treatments for diabetes complications, will be published in this month’s Cell Metabolism.
Cellular repair is harder for those with Type 1 diabetes, which winds up leading to complications in the heart, kidneys, eyes and nerves. Staving off complications could be a game-changing move in improving the lives of type 1 diabetics.
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“Even with very good glycemic control, people with Type 1 diabetes can still develop complications that impact their ability to work and quality of life,” said Dr. Rohit Kulkarni, a researcher at Joslin Diabetes Center and Harvard University and lead author of the study. “If we could find therapies that detect complications at an early stagy stage, people with diabetes could lead healthier, more productive lives.”
It could also prove marketable fodder for the pharmaceutical industry, should this breakthrough lead to an effective diagnostic or therapeutic. A 2010 PLOS study found that type 1 diabetes cost the country at the time $14.4 billion in medical costs and loss income. But if the disease were eliminated with therapeutic intervention — and this could include complication control, most likely — some $422.9 billion in medical costs over type 1 diabetics’ lifetime could be avoided.
The Type 1 diabetes market is projected to double in the decade after 2013, so that will hit $13.6 billion by 2023. Indeed, diabetes drug pricing is going up, despite a general lack of approved advancements on the market.
The study in Cell Metabolism used the induced pluripotent stem (iPS) cells of patients who have had type 1 diabetes for 50 years or more. Through genetic analysis, researchers found alternations in the DNA damage checkpoint pathway that monitors the cell repair process. Since the type 1 diabetics had a faulty repair process, their cells were more prone to die – leading to the complications. This was particularly true among nerve cells, particularly when comparing patients who had severe complications to those with mild complications.
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The genetic analysis found higher concentrations of an RNA molecule called miR200 in patients with severe complications. So, when patients reduced the expression of miR200 in the iPS and skin cells, DNA damage was reduced.
The Joslin researchers plan to differentiate the diabetics’ iPS cells into kidney, eye and vascular cells, and learn more about how complications develop. This could lead to a more efficient way to test which medications are effective in different patients.
“We need to figure out the exact mechanisms by which miR200 regulates the DNA repair process and also determine if miR200 can be detected in the bloodstream and serve as an effective biomarker for complications,” Kulkarni said.
