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Zinc chelation may be able to deliver drug to insulin-producing cells

By delivering a drug directly to beta cells, researchers may be able to spur insulin production and potentially develop a diabetes therapy in the future.

Stanford researcher Justin Annes, MD, PhD, wants to know how to make more beta cells, those insulin-producing cells that live in the pancreas. More beta cells would make more insulin, and more self-made insulin would be a huge boon to millions of diabetics worldwide.

He and others figured out a first step: how to make the beta cells replicate. But then other cells would replicate, too, and that could cause any number of complications.

A Stanford Medicine press release picks up the tale:

Then Annes had a thought: Researchers have known since the 1940s that beta cells collect about 1,000 times more zinc than surrounding tissue cells. Researchers have mostly used that fact as a way to stain and visually identify beta cells in pancreatic tissue samples. But Annes reasoned that if he could somehow get a regenerative drug to seek out zinc, he could get it to beta cells.

With help from Timothy Horton, a graduate student in chemistry, and Mark Smith, PhD, senior research scientist at Stanford ChEM-H and director of its Medicinal Chemistry Knowledge Center, they figured out how to do just that.

They showed that by attaching a regenerative drug to zinc-chelating agent, which bonds to zinc, they were able to concentrate the drug, and therefore the regeneration it triggered, in the beta cells, rather than in other cells.

The research appears in Cell Chemical Biology.

Although hopeful, the work is in the "earliest stages," Annes said. "This is the first demonstration of a selectively delivered replication molecule in beta cells and it's not sufficient for therapeutic applications."

In the future, Annes and his colleagues plan to refine their method so it more precisely targets only beta cells.

Image of mouse pancreatic islet (where beta cells are located) with insulin in red by Jakob Suckale

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