Stanford researchers identify new molecular target for diabetes therapy

London, Oct 13 (ANI): Artificially activating a key molecular pathway responsible for the natural decrease in the proliferation of insulin-producing cells that occurs as a person ages could one day lead to a new way to combat diabetes, say researchers at the Stanford University School of Medicine.

The researchers found that, in mice and humans, the pathway is governed by the expression of a molecule called platelet-derived growth factor receptor.

PDGF-receptor expression declines over time in mice and humans in a pattern that parallels the decrease in the proliferation of pancreatic beta cells, which produce insulin to control blood sugar levels.

It's been known for some time that beta cell proliferation in the pancreas, which is robust in newborn and young animals, decreases dramatically with age.

The expression of one molecule known to be involved, Ezh2, declines over time in a similar manner. However, it was not known what controlled the changes in Ezh2 expression levels in beta cells.

The researchers found that the expression of PDGF receptors was also reduced in pancreatic islet cells from juvenile mice in a pattern similar to the reduction in beta cell proliferation.

When they blocked the expression of PDGF receptors in laboratory mice, they found that young animals (2 to 3 weeks old) made less Ezh2 and had significantly fewer beta cells than control animals. They also had slightly elevated blood sugar levels and were less effective than control animals in disposing of blood sugar when challenged with high glucose.

Adult animals lacking expression of the beta cell PDGF receptor were also less able than their peers to regenerate beta cells that were artificially damaged by a chemical compound, and they became severely diabetic after such treatment.

"We're hopeful that soon we might be able to manipulate this pathway in a therapeutic way in humans," said senior author and professor of developmental biology Seung Kim, MD, PhD.

"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," he said.he researchers said their study revealed that there were some pathways that have not been explored in human beta cells that underlie the age-related loss of beta cell proliferation.

"This gives us a handhold onto a vaster problem: how to control human beta cell proliferation in a therapeutic way," said Kim.

The finding appears online Oct. 12 in Nature. (ANI)


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