For the first time scientist transformed human stem cells into mature insulin-prodcing cells. This is a major major breaktrough of UC San Francisco researchers, in the effort to develop cure for type 1 (T1) diabetes.
In type 1 diabetes, the body does not produce insulin. The body breaks down the carbohydrates you eat into blood glucose (also called blood sugar), which it uses for energy. Insulin is a hormone that the body needs to get glucose from the bloodstream into the cells of the body.
"We can now generate insulin-producing cells that look and act a lot like the pancreatic beta cells you and I have in our bodies. This is a critical step towards our goal of creating cells that could be transplanted into patients with diabetes,” said Matthias Hebrok, PhD, the Hurlbut-Johnson Distinguished Professor in Diabetes Research at UCSF and director of the UCSF Diabetes Center.
T1 diabetes is an autoimmune disorder that destroys the insulin-producing beta cells of the pancreas, typically in childhood. Without insulin’s ability to regulate glucose levels in the blood, spikes in blood sugar can cause serious organ damage and eventually death. The condition can be managed by taking regular shots of insulin with meals, but people with type 1 diabetes still often experience serious health consequences like kidney failure, heart disease and stroke.
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A pancreas transplant from a deceased donor is possible. However, doctors said they are rare and the wait time is long. Doctors said that even then, the transplant may fail for a number of reasons.
Researchers said the cells they were able to transform were transplanted into mice and found that the cells were functional in a matter of days and were producing insulin in response to blood sugar.
Doctors must still conduct more research, and it is unclear if the discovery will lead to a full cure just yet. However, they are hopeful for the future.
“We’re finally able to move forward on a number of different fronts that were previously closed to us,” Hebrok said. “The possibilities seem endless.”
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