Type 1 diabetes: Reprogramming liver cells may lead to new treatments
Researchers have discovered a way to reprogram mouse liver cells into precursor pancreatic cells by changing the expression of a single gene. They suggest that the finding is an important step toward showing that reprogramming liver cells might offer a way forward for the treatment of type 1 diabetes in humans.
The team - led by researchers from the Max Delbrück Center for Molecular Medicine in Berlin, Germany - reports the study in the journal Nature Communications.
Diabetes is a chronic disease that develops either when the body cannot make enough insulin, or when it cannot effectively use the insulin that it does make. Insulin is a hormone that regulates blood sugar, or glucose, and it helps to convert glucose from food into energy for cells.
Uncontrolled diabetes leads to high blood sugar, or hyperglycemia, which over time causes serious damage to many parts of the body, including the heart, blood vessels, nerves, eyes, and kidneys.
In the United States, an estimated 29.1 million people have diabetes, including 8.1 million who are undiagnosed.
The most common type of diabetes is type 2, in which the body cannot use insulin effectively. Type 1 diabetes, in which the body does not make enough insulin, accounts for around 5 percent of diabetes cases in adults.
The new study is likely to interest researchers developing treatments for type 1 diabetes. In people with type 1 diabetes, the immune system attacks the insulin-producing beta cells of the pancreas.
The advantages of using liver cells
Researchers in regenerative medicine are exploring ways to generate new populations of pancreatic beta cells as a possible avenue for the treatment of type 1 diabetes.
The new study concerns a method called cell reprogramming, in which it is possible to convert one type of cell into another type of cell, by tweaking genes.
An obvious source of cells for reprogramming into insulin-producing beta cells might be other types of cell in the pancreas.
In their study paper, the researchers mention other research that shows such pancreatic cells display a high degree of the necessary "cellular plasticity."
However, the researchers chose to focus on liver cells because, from a clinical perspective, they offer important advantages over pancreatic cells; for example, they are more accessible and abundant.
They also cite studies that have partially corrected hyperglycemia in diabetic mice by reprogramming liver cells into pancreatic beta cells.
The new study shows how just by changing the expression of a single gene called TGIF2, the team was able to coax mouse liver cells to take on a less specialized state and then stimulate them to develop into cells with pancreatic features.
