The article presents a promising strategy to prevent or slow the progression of Type 1 diabetes by targeting an inflammation-related protein known to drive the disease. Researchers have found that applying a molecular method to block inflammation signaling through the tyrosine kinase 2 (TYK2) protein reduces harmful inflammation in the pancreas, protecting insulin-producing beta cells and calming the immune system’s attack on those cells.

Type 1 diabetes is a lifelong condition where the immune system mistakenly attacks and destroys insulin-producing beta cells in the pancreas. This leads to high blood sugar levels, requiring ongoing insulin therapy and careful monitoring to avoid severe health complications.

The study, co-led by Indiana University School of Medicine researchers, presents a potential new strategy using a medication that inhibits TYK2, which is already approved for the treatment of psoriasis, an autoimmune condition causing skin inflammation. This finding is exciting because there is already a drug on the market that can do this for psoriasis, which could help move toward testing it for Type 1 diabetes more quickly.

Past genetic studies have shown that people with naturally lower TYK2 activity are less likely to develop Type 1 diabetes, further supporting the group’s approach for future treatments using this TYK2 inhibitor approach.

The researchers hope their findings will support future clinical trials to safely assess the efficacy of a new drug or drug combination in humans. They emphasize the importance of initiating translational studies to evaluate the impact of TYK2 inhibition alone or in combination with other already approved drugs in individuals at-risk or with recent onset Type 1 diabetes.

The study’s lead author, Farooq Syed, PhD, notes that their preclinical models suggest that the treatment might work in people as well. The next step is to initiate translational studies to evaluate the impact of TYK2 inhibition alone or in combination with other already approved drugs in individuals at-risk or with recent onset Type 1 diabetes.

The research team hopes to support future clinical trials to safely assess the efficacy of a new drug or drug combination in humans, offering hope for a potential treatment approach for Type 1 diabetes.

The discovery of how impaired mitochondrial dynamics and quality control mechanisms contribute to insulin resistance related to type 2 diabetes has shed new light on the complex interplay between mitochondria and metabolic health. Researchers at Pennington Biomedical Research Center have made groundbreaking findings, published in the Journal of Cachexia, Sarcopenia and Muscle, that reveal critical insights into how certain enzymes regulate mitochondrial dynamics within skeletal muscle.

The study, led by Dr. John Kirwan, Executive Director of Pennington Biomedical, focused on the significance of deubiquitinating enzymes (DUBs) in maintaining mitochondrial quality control. The research team found that impaired mitophagy, the process by which cells remove damaged mitochondria, can lead to mitochondrial fragmentation as a compensatory mechanism. This adaptation allows skeletal muscle cells to sustain function despite metabolic challenges.

In individuals with type 2 diabetes, a specific protein called dynamin-related protein 1 (DRP1) is overactive, causing an imbalance in mitochondrial dynamics. Furthermore, the team discovered that certain DUBs interfere with mitophagy, making it more difficult for muscles to use insulin properly. This intricate interplay between mitochondria and insulin sensitivity has significant implications for our understanding of type 2 diabetes.

The research findings advance the knowledge on how impaired mitochondrial dynamics and quality control contribute to skeletal muscle insulin resistance and the manifestation of type 2 diabetes. Moreover, they provide crucial evidence that DUB antagonists may play a vital role in preventing or treating type 2 diabetes.

“Our study highlights the complex relationship between mitochondria and insulin,” said Dr. Kirwan. “We are excited about the potential for future interventions aimed at improving metabolic health, particularly in the context of type 2 diabetes.”

The world of tissue engineering has just taken a significant leap forward with the advent of Freeform Reversible Embedding of Suspended Hydrogels (FRESH) 3D bioprinting. This innovative technique, developed by Carnegie Mellon’s Feinberg lab, allows for the printing of soft living cells and tissues with unprecedented structural resolution and fidelity. The result is a microphysiologic system entirely made out of collagen, cells, and other proteins – a first-of-its-kind achievement that expands the capabilities of researchers to study disease and build tissues for therapy.

Traditionally, tiny models of human tissue have been made using synthetic materials like silicone rubber or plastics, but these cannot fully recreate normal biology. With FRESH bioprinting, researchers can now create microfluidic systems in a Petri dish entirely out of collagen, cells, and other proteins – a major breakthrough that will revolutionize the field.

“We’re hoping to better understand what we need to print,” said Adam Feinberg, a professor of biomedical engineering and materials science & engineering at Carnegie Mellon University. “Ultimately, we want the tissue to better mimic the disease of interest or ultimately, have the right function, so when we implant it in the body as a therapy, it’ll do exactly what we want.”

The implications of this technology are vast, with potential applications in treating Type 1 diabetes and other diseases. FluidForm Bio, a Carnegie Mellon University spinout company, has already demonstrated that they can cure Type 1 diabetes in animal models using this technology, and plans to start clinical trials in human patients soon.

As Feinberg emphasized, “The work we’re doing today is taking this advanced fabrication capability and combining it with computational modeling and machine learning… We see this as a base platform for building more complex and vascularized tissue systems.”

With FRESH bioprinting, the possibilities are endless. This technology has the potential to change the face of medicine and improve countless lives. As researchers continue to push the boundaries of what is possible, one thing is certain – we will witness some incredible breakthroughs in the years to come.