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Health Rounds: 3D printed insulin-producing cells show promise for type 1 diabetes in lab tests
By Nancy Lapid - 7/2/2025
(This is an excerpt of the Health Rounds newsletter, where we present latest medical studies on Tuesdays and Thursdays.)
By Nancy Lapid
(Reuters) -Insulin-producing human pancreas cells can be manufactured with 3D printers, researchers reported at the International Transplant Congress underway in London.
Using a bio-ink made from human pancreatic tissue from which all cellular components had been removed, and alginate - a substance derived from seaweed - they printed human pancreatic islet cells. The printed cells remained alive and functional in test tubes for up to three weeks, maintaining strong insulin responses to glucose and showing real potential for future clinical use, the researchers said.
While current methods of isolating islet cells for transplantation strip away the structural scaffold that supports the cells, the bio-ink retains key components of that extracellular matrix, thereby improving the cells’ survival and function, the researchers said.
The printed cells were more efficient than standard islet cell preparations at releasing insulin when exposed to glucose. By day 21, the bio-printed islets showed a stronger ability to sense and react to blood sugar levels, and they maintained their structure without clumping or breaking down.
In traditional islet-cell transplants, done in patients with type 1 diabetes who experience dangerous and unpredictable low blood sugar episodes, islet cells from human donors are infused into the liver. The 3D-printed islets would be implanted under the skin using local anesthesia and a small incision, which could be safer and more comfortable option for patients, the researchers said.
The team is now testing the bio-printed cells in animals and exploring long-term storage options that could make the therapy widely available.
“This is one of the first studies to use real human islets instead of animal cells in bio-printing, and the results are incredibly promising,” study leader Quentin Perrier of Wake Forest University School of Medicine in North Carolina said in a statement.
“It means we're getting closer to creating an off-the-shelf treatment for diabetes that could one day eliminate the need for insulin injections.”
GENE EDITING BREAKTHROUGH IN CELLS’ ENERGY FACTORIES
Incurable disorders of mitochondria, the energy-producing “factories” inside of cells, may one day be addressed by gene therapies, lab experiments suggest.
Mitochondria – specialized structures within cells - have their own DNA, separate from the DNA in the cell’s nucleus. Mutations in mitochondrial DNA can cause a variety of debilitating conditions affecting multiple organs, particularly those that require high energy, such as the brain, liver, heart, muscles, and kidneys.
Existing gene editing tools like CRISPR have not been useful for these disorders because they can’t efficiently pass through the mitochondrial membranes.
“Using a new kind of gene editing tool, we were able to fix DNA mistakes that cause mitochondrial disease,” said study leader Dr. Martijn Koppens from the University Medical Center Utrecht in the Netherlands.
To cut and paste pieces of DNA, the new tool uses different mechanisms and components than CRISPR. For example, instead of the Cas protein, the new tool, called DdCBE, uses an inactive version of a bacterial toxin as its molecular scissors.
To deliver the “scissors” to the mitochondria, the tool uses mRNA encapsulated in tiny lipid particles, a transport method also used to deliver COVID-19 vaccines.
As reported in PLoS Biology, Koppens’ team successfully used their tool to introduce a mutation into a gene in liver cell mitochondria, thereby disrupting energy production in the cells.
They were also able to correct a mutation in mitochondria from a patient with a genetic kidney disorder.
“I envision that in the near future, mitochondrial gene editing will be used to generate accurate mitochondrial disease models, which will transform basic research as well as therapy development,” Koppens said.
BLOOD THINNERS CAN OFTEN BE STARTED SOON AFTER A STROKE
Blood thinner therapy need not be delayed in most patients with a recent stroke attributable to an irregular heartbeat, according to a new analysis.
Pooling data from four randomized trials involving nearly 5,500 patients with atrial fibrillation and a recent stroke, researchers found that starting direct oral anticoagulants - which prevent formation of blood clots - within four days was safe and effective.
These drugs include Johnson & Johnson’s Xarelto or Eliquis from Bristol Myers Squibb and Pfizer.
Atrial fibrillation can lead to blood clots in the heart that dislodge and travel to the brain, causing a stroke. Blood thinners can prevent clots, but they also increase the risk of bleeding in the brain, so it has been common practice to hold off for a while after a stroke before starting them.
Based on the safety observed in the current analysis, “the benefits of early initiation of blood-thinning treatment are clear," study leader Nick Freemantle of University College London said in a statement. "This approach ensures that crucial treatments are not delayed or missed, particularly for patients who are discharged from the hospital."
Patients were split into two groups, with 2,691 receiving the blood thinners within 4 days and 2,750 starting the pills on day 5 or later.
The incidence of either recurrent strokes from blood clots or strokes from bleeding in the brain was 2.1% with early anti-coagulation administration and 3.0% with delayed treatment, researchers reported in The Lancet.
There was no increase in brain bleeding in the early-treatment group. However, few patients in the trial had experienced strokes that extensively damaged the brain, which would have increased the bleeding risks associated with starting the blood thinners right away.
An editorial published with the study concludes that overall, the findings favor early initiation of oral anticoagulation in patients with strokes related to atrial fibrillation, especially those with smaller amounts of brain damage.
However, the editorial noted some additional factors for providers to consider.
“Adherence to strict predefined early or late initiation thresholds might oversimplify the complexity" of deciding when to start blood thinners, it noted. It said there should be an assessment of other co-morbidities, including advanced age, other medications being taken and frailty, when delayed blood thinner therapy "might derive increased benefit.”
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(Reporting by Nancy Lapid; additional reporting by Shawana Alleyne-Morris; editing by Bill Berkrot)