The way to manage Type 1 diabetes, an autoimmune disease that causes the body to attack its own insulin-producing cells, has always been through regular insulin injections. But what if diabetes could actually be cured?
Scientists have moved one step closer to what they hope could become a cure for Type 1 diabetes, a disease affecting an estimated 3 million Americans, usually diagnosed in childhood or early adulthood, according to the Juvenile Diabetes Research Fund.
They did this by transforming already existing cells of the pancreas into beta cells, the type that make insulin and which are eventually destroyed by diabetics’ immune systems. The experiment was performed in mice. But if replicated in humans, it could potentially free up diabetics from the constant monitoring of blood sugar levels and regular injections of insulin that are necessary to keep them alive.
“This is an ongoing field of investigation,” said Dr. Fred Levine, director of the Children’s Health Research Center at the Sanford-Burnham Medical Research Institute in La Jolla, California, who led the research study. “There’s a tremendous amount of interest in trying to generate new beta cells because they’re a major target in Type 1 diabetes.”
A paper detailing the team’s research was published online Thursday in the journal Cell Death and Disease.
Researchers gave diabetic mice a peptide called caerulein, which was originally discovered in the skin of Australian Blue Mountains tree frogs. Really, it’s just a tiny protein that happens to stimulate the secretion of digestive enzymes into overdrive.
Levine and his team gave caerulein to diabetic mice whose beta cells were almost entirely destroyed, a similar state to humans with Type 1 diabetes. The peptide caused the alpha cells — a different type of pancreatic cell that’s found right next to the beta cells — to regenerate into insulin-producing beta cells in the mice. However, it didn’t have the effect of transforming alpha cells into beta cells in normal mice.
Next, in order to test whether the same regeneration might occur in humans, Levine’s team administered caerulein to human pancreatic tissue and found that alpha cells also transformed into beta cells, regardless of how young or old the tissue was.
“It’s a somewhat surprising thing, that in the adult, our cells retain the ability to convert back and forth to other cell types, with an appropriate stimulus,” Levine said.
But getting the body to make more of those pancreatic beta cells is only part of the equation. Since Type 1 diabetes is an autoimmune disease, even if the pancreas regenerates more beta cells, the body would still try to thwart them.
So his team is partnering with immunologists to figure out how to temper the body’s autoimmune response.
The other problem, Levine said, is that if humans were to be given this particular peptide at high enough levels to create beta cells, it would likely induce pancreatitis.
The next step, he said, is to more closely identify how caerulein induces transformation in the alpha cells to create a more targeted drug, and eventually move on to human clinical trials, but the field of converting pancreatic cells into those that produce insulin is extremely new.
“We’re working to understand exactly what is the mechanism by which [the peptide] causes the alpha cells to turn into beta cells so we can use a more targeted approach.”