Insulin implant could transform diabetes treatment

A living implant has kept diabetic animals’ blood sugar in range by making insulin automatically inside the body.

If the same approach works in people, it could replace daily injections with an internal system that adjusts itself.

Proof in animals

Animal trials put the implant under stress, because blood sugar levels rose and fell as the animals ate and moved.

From that up-and-down testing, engineers at the Technion showed the device could dose insulin on its own.

In diabetic mice, Technion collaborators reported one year of steady blood sugar control in the paper.

Keeping the implant working that long required stopping the body from sealing it off, and that challenge shaped every material choice.

Cells that sense sugar

Inside the implant, living cells handled the job a pancreas normally does, reacting quickly when blood sugar climbed.

As blood sugar rose, beta cells, the pancreas cells that make insulin, released stored hormones that helped muscles absorb sugar.

After sugar dropped, the same cells slowed insulin release, reducing the risk of a dangerous low.

Maintaining that balance depended on enough oxygen and nutrients reaching the cells through their protective barrier.

When immune walls form

Once any device goes into the body, the immune system can react by building a tight coat of scar tissue.

In this foreign body response, a defense reaction that walls off implants, immune cells crowd the surface and block flow.

For islet transplantation, doctors often rely on immunosuppressants, medicines that damp immune attacks, and federal guidance lays out why.

Avoiding those drugs means the implant must stay open to nutrients while still hiding the cells from attack.

Preventing scar overgrowth

To stop that sealing, the team tucked slow-dissolving drug crystals into the same capsule that carried insulin-making cells.

As the crystals dissolved, they released medicine locally, preventing macrophages, immune cleanup cells that can drive scarring, from piling on.

Instead of shutting down immunity across the body, the drug worked at the implant surface where overgrowth begins.

Even with that local protection, long-term success still depends on matching the cell source to the recipient’s immune system.

When species lines matter

In nonhuman primates, the system behaved differently depending on whether implanted cells came from the same species.

Allogeneic cells – from a donor of the same species – stayed sugar-responsive after one month without systemic immune suppression.

Xenogeneic human stem cell-derived cells – from a different species source – triggered heavy overgrowth and failed inside primate tissue.

That failure tracked with the adaptive immune system. This targeted arm learns new threats and is harder to calm locally.

How devices work today

A report highlighted one difference patients notice first, because nothing had to be worn on the skin.

“Unlike existing technology, the implant operates without the need for external pumps or patient monitoring,” noted the report.

On today’s skin-worn gear, an artificial pancreas system links a sensor, software, and a pump to adjust insulin delivery.

Removing that equipment could cut down daily dosing decisions, but a living implant must match or beat that safety record.

Hurdles before human trials

In 2023, 40.1 million Americans had diabetes, and the Centers for Disease Control and Prevention report puts that number in plain view.

Before human trials, developers must prove the implant can be placed safely, then removed if it overproduces insulin.

Securing a steady supply of cells also matters, because donor tissue is limited and lab-grown cells must stay predictable.

Until those basics are solved, an implant that works in animals will remain a prototype rather than a treatment.

Beyond diabetes targets

Beyond diabetes, the same capsule could hold cells engineered to release missing proteins at a steady rate.

By swapping the insulin program for another, the cells could drip out clotting factors for hemophilia or enzymes for rare disorders.

Because the cells would make the drug inside the body, patients might avoid repeated infusions or frequent dose changes.

Any new use would still face the same immune and safety barriers, since the body reacts to cells and materials.

Building living medicines

Turning cells into medicine changes the job of a drug from a pill to a living system that responds to cues.

Instead of shipping finished insulin, labs would ship controlled cells, and regulators would track both device materials and biology.

Long-term monitoring would matter, because living cells can mutate, slow down, or grow too fast under stress.

Success would open a path to implants that manage chronic disease quietly, but failure could be hard to reverse.

Future development path

Animal results showed that living insulin cells can regulate sugar inside the body, yet immune barriers still determine longevity.

Next steps will demand careful human trials, stronger immune protection, and clear ways to switch the implant off.

The study is published in Science.

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