Saturday Morning Research Review – March 11, 2017

The “race” to develop the first FDA-approved insulin dosing algorithm by Adam Burrack, PhD In the vast majority of our blogs, I’ve focused on the fundamental problem underlying type 1 diabetes (T1D), destruction of insulin-producing beta cells by the immune system. I am fascinated by the biology underpinning how the immune system mis-identifies beta cells […]

Saturday Morning Research Review – March 4, 2017

Key differences between type 1 diabetes and type 2 diabetes: autoantibodies and inflammation by Adam Burrack, PhD It’s a persistent question when comparing type 1 diabetes and type 2 diabetes: they require the same treatment – insulin injections – so how similar are the disease processes leading to beta cell death? In general this is […]

Saturday Morning Research Review – February 25, 2017

Skeletal muscle regenerative capacity may be decreased with type 1 diabetes By Adam Burrack, PhD, and Daniel Schneider, MSc A recent article in Diabetes describes an interesting finding about skeletal muscle in insulin-deficient diabetic mice and people with type 1 diabetes. These findings may have direct implications for how people with type 1 diabetes may […]

Saturday Morning Research Review – February 11, 2017

Engineered beta cells may be a fourth path to restored euglycemia for diabetic patients by Adam Burrack, PhD In our “science of diabetes” series, I’ve previously described a couple of neat “engineering solutions” to insulin infusion and diabetes management. One of these was “smart insulin” about Danny Chou and the smart insulin initiative by JDRF. The […]

Saturday Morning Research Review – February 4, 2017

An additional hybrid insulin peptide as target of autoreactive T cells by Adam Burrack, PhD Readers of our “science of diabetes” blog will remember a news story about a year ago, in which researchers at the Barbara Davis Center in Denver, Colorado and in Australia collaborated to demonstrated the clinical relevance of so-called hybrid insulin […]

Saturday Morning Research Review – January 28, 2017

Inflammation promotes intra-pancreas neuron signaling which promote Th17 cells which promote beta cell destruction by Adam Burrack, PhD In a previous post about zonulin, I described how our diet influences gut permeability and may play a role in gut-directed autoimmunity. In that post I described the hypothesis that our diet influences the immune system’s response […]

Saturday Morning Research Review – January 21, 2017

Defects in development of regulatory T cells promote autoimmune disease by Adam Burrack, PhD Biology is a confusing beast sometimes. In particular the immune system. In particular the checks and balances between different branches of the immune system, each with different goals. Effector T cells protect the organism from exterior threats – potentially at the […]

Saturday Morning Research Review – January 14, 2017

Finding autoreactive T cells within type 1 diabetic pancreas samples by Adam Burrack, PhD We continue our series of descriptions of research output of the Human Islet Research Network. As a brief reminder, this consortium of NIH-funded researchers are working to develop methods to delay beta cell death, manipulate the immune system to prevent beta […]

Saturday Morning Research Review – January 7, 2017

Pancreatic islet transplant survival promoted by co-transfer of immune suppressive cells               by Adam Burrack, PhD Pancreatic islet transplants represent a potential cure for type 1 diabetes, but are limited both by resources – vanishingly few donor organs are available – and biology – we cannot prevent chronic transplant rejection. I recently described some of the […]

Saturday Morning Research Review – December 17, 2016

The double-edged sword of cancer immunotherapy and autoimmunity by Adam Burrack, PhD “Immune checkpoint” therapy is the current cutting edge to treat cancer. Since cancer is the mirror image of autoimmunity – in cancer we want to promote a response in the presence of strong local suppression, in autoimmunity we want to stop a response […]