Jackson Lab announces diabetes breakthrough Researchers repair defective cells in mice

BAR HARBOR – Dr. Dave Serreze of The Jackson Laboratory thinks that he and his research team may have discovered the key that will unlock some of the genetic mysteries of type 1 diabetes.

The scientists have figured out a way to fix defective, diabetes-causing cells in laboratory mice before the disease ever has a chance to develop.

“It’s such a complicated disease, but we’ve made a major contribution as to why these cells cause diabetes and why they develop,” Serreze said Monday. “Hopefully, we can find a way to correct the problem.”

Type 1 diabetes, formerly known as juvenile onset diabetes, is a genetic ailment that takes a tough toll on its victims when it causes them to lose their ability to produce insulin. It is diagnosed primarily in children and young adults, and may affect as many as 2.8 million Americans, according to the American Diabetes Association.

Without insulin, the body can’t use sugar, the basic fuel for cells. Though this inability can be managed through careful monitoring of blood glucose levels and injection of insulin, that’s not a panacea, the scientist said. Long-term effects of type 1 diabetes can include heart disease, blindness, nerve damage and kidney damage.

“This is not an easy disease to live with, by any stretch of the imagination,” Serreze said. “If you see what these young kids are going through and how bravely they face it, it would blow you away.”

His 10-year-old research project will continue for at least four more years, thanks to the $1.3 million government grant he has just received.

The research team has been studying antigen-presenting cells, or APCs, which show the body’s white blood cells what to fight off and what to leave alone, a process called “tolerance induction.”

In type 1 diabetes, the white blood cells go haywire and destroy cells in the pancreas that create insulin.

“The analogy I use is that the tolerance induction process is like a college-level course, but the teachers themselves, in this case the antigen-presenting cells, have not gotten out of the second grade,” Serreze said. “We’re trying to understand the genetic basis for this developmental defect.”

As Serreze and his researchers have worked to unlock the reasons this defect occurs, they have found a way to solve the problem in laboratory mice that have been engineered to develop type 1 diabetes.

Yi-guang Chen, a postdoctoral fellow from China, discovered a corrective protein that fixes the APCs. For the moment, the protein is called “Factor Yi” after the researcher.

Though Factor Yi’s different components have yet to be identified, it is a big step for diabetes research and provides a beacon of hope for those carrying the genetic programming to develop the disease in the future.

The team’s next few years of research will study the effectiveness of the corrective protein. Down the line, Serreze said, the research that has been performed on lab mice will be transferred to people.

“The whole key is if we could identify people before they have diabetes,” Serreze said. “Identify and prevent. I would be absolutely elated if we could do that. It would put us out of work, but I wouldn’t care.”