Could THIS be a cure for diabetes? Scientists create insulin-making pancreatic cells that escape the disease’s attacks and can be transplanted into patients
- Researchers created clusters of beta-like cells that are produced in the pancreas from stem cells
- Adding two proteins to the cells ‘turbo-charged’ them to produce insulin and keeping the immune system from attacking them
- When they were transplanted into diabetic mice, the clusters controlled blood sugar and were not attacked by the immune system
- This means the clusters could be transplanted into type 1 diabetes patients without having to give them immunosuppressive drugs
Clusters of insulin-producing pancreatic cells that can be given to type 1 diabetics could be the first step towards a cure, researchers claim.
From stem cells, a team at the Salk Institute in La Jolla, California created beta-like cells that produce insulin in response to glucose.
When these cells were transplanted into diabetic mice, controlled blood glucose and the rodents didn’t need to be given immunosuppressive drugs.
The treatment is experimental and in early stages of testing, but scientists believe that its powerful effect could be a game-changer in the treatment of diabetes.
A new study from the Salk Institute found that adding two proteins to the beta-like cells ‘turbo-charged’ them to produce insulin and kept the immune system from attacking them.
According to the Centers for Disease Control and Prevention, 30.3 million Americans – about 9.4 percent of the population – suffers from diabetes.
However, only about five to 10 percent of those with diabetes have type 1.
It occurs when there are too few beta cells in the pancreas to produce insulin or when they produce very little insulin, the hormone needed to get glucose from the bloodstream into cells.
When left untreated, diabetes can result in serious health complications such as kidney damage, eye damage, heart disease, stroke and even vision loss.
‘Most type 1 diabetics are children and teenagers,’ said Dr Ronald Evans, a professor and director of the Gene Expression Laboratory at the Salk Institute.
‘This is a disease that is historically hard to manage with drugs. We hope that regenerative medicine in combination with immune shielding can make a real difference in the field by replacing damaged cells with lab-generated human islet-like cell clusters that produce normal amounts of insulin on demand.’
WHY DO DIABETICS INJECT INSULIN?
Insulin is a hormone made in the pancreas, an organ in your body that helps with digestion.
Insulin helps your body use glucose – which comes from sugar in the food and drinks you consume – for muscle energy.
Glucose is initially absorbed by the gut from food and passed into the blood, where the body decides what to do with it.
Insulin makes this decision by regulating how much sugar moves from the blood into the blood cells, muscles or fat cells, where it can be used up or stored.
But diabetes can mean the pancreas does not make any insulin, it doesn’t make enough, or the insulin it does make doesn’t work properly.
This can lead to the levels of sugar in the blood becoming dangerously high or low – which can cause fatigue, feeling hungry or thirsty, or in extreme cases life-threatening coma.
To avoid this and stop blood sugar from getting too high, diabetics can inject insulin into their body as a medication to bring their blood sugar down.
Many Type 1 diabetes patients undergo transplants of pancreatic beta islets – clusters of cells that make insulin and other hormones – from donor tissue.
While this can provide a cure, it also requires them to take immunosuppressing drugs for the rest of their lives to avoid rejection.
Previously, the team had discovered that a protein-coding gene called ERR-gamma ‘turbo-charged’ stem-cell-derived beta cells that produce insulin in response to glucose.
‘When we add ERR-gamma, the cells have the energy they need to do their job,’ said co-author Dr Michael Downes, a Salk senior staff scientist.
‘These cells are healthy and robust and can deliver insulin when they sense high glucose levels.’
For the new study, published in Nature, the team focused on how to grow these beta-like cells in an environment similar to the human pancreas.
They found another protein-coding gene, WNT4, turns on a switch that allows the beta-like cells to attain their fully-functional state that mimics islets in the pancreas.
To prevent immune rejection, they used the protein PD-L1, which keeps immune cells from attacking non-harmful cells in the body.
‘By expressing PD-L1, which acts as an immune blocker, the transplanted organoids are able to hide from the immune system,’ said first author Dr Eiji Yoshihara, a former staff scientist at the Salk Institute.
When these completed clusters were transplanted into diabetic mice, they controlled blood glucose control and were not attacked by the immune system.
The team hopes to conduct more experiments in mice and prove that it’s safe for humans as well.
‘We now have a product that could potentially be used in patients without requiring any kind of device,’ Evans said.