Researchers identify molecular pathway that may become target of type 1 diabetes and type 2 diabetes medications
There are many causes of both type 1 diabetes and type 2 diabetes. Now, a team of researchers from Stanford University may have found a common treatment for both disorders.
The group reported in the journal Nature
that a molecule called platelet-derived growth factor, or PDGF, is responsible for the growth of new insulin-producing beta cells in the pancreas. This discovery could lead to the development of new medications that allow the pancreases of individuals with either type of diabetes to produce more insulin, achieving better glucose control.
The researchers noted that the activity of this cellular pathway decreases over time. Older people tend to have fewer beta cells than younger people. This is one reason why seniors are at a significantly higher risk of developing type 2 diabetes. However, until the present study, it was not entirely clear why this was.
For the study, the researchers examined mice that were genetically engineered to have low expression of PDGF. When they did this, they found that the animals had lower levels of molecules associated with cell growth and fewer beta cells in their pancreases.
However, when the researchers artificially stimulated the PDGF molecule, the mice began to grow new beta cells at a rapid rate. This led to significant improvements in blood sugar control.
"This work revealed that there are some pathways that haven't been explored in human beta cells that underlie the age-related loss of beta cell proliferation," said lead researcher Seung Kim. "This gives us a handhold onto a vaster problem: how to control human beta cell proliferation in a therapeutic way."
There is a strong possibility that the findings could be used to develop new medications that benefit both type 1 diabetics and type 2 diabetics.
In type 1 diabetes, a person's immune system begins attacking and destroying beta cells, leaving the individual's body unable to keep up with demands for insulin. By activating the PDGF pathway, these individuals may be able to regrow beta cells, making them less reliant on insulin.
Many people who have type 2 diabetes developed the condition as they got older. This may be partially due to the fact that the PDGF pathway has slowed down and they are no longer growing new beta cells. However, stimulating the molecule may enable them to achieve better blood sugar management by producing more of these vital cells.
Despite the fact that both types of diabetes have such different causes and effects, Kim thinks that a single medication developed based on the findings could benefit them both.
"We're hopeful that soon we might be able to manipulate this pathway in a therapeutic way in humans," he said. "Perhaps by rekindling its expression and then activating it through a drug we could give in an injection or through some other route. This could be a kind of one-two punch against diabetes."