Beta Cell Stress Could Trigger Type 1 Diabetes @JDRF

Before T1d Stresses patients, stress on the beta cells may trigger T1D. Which matters because understanding how it works help find cures. So knowing what you don't know helps.

Study provides important clue in type 1 diabetes; could help scientists identify and validate potential drug targets to alleviate ER stress and preserve beta cell mass in T1D
In type 1 diabetes (T1D), pancreatic beta cells die from a misguided autoimmune attack, but how and why that happens is still unclear. Now, JDRF-funded scientists from the Indiana University School of Medicine have found that a specific type of cellular stress takes place in pancreatic beta cells before the onset of T1D, and that this stress response in the beta cell may in fact help ignite the autoimmune attack. These findings shed an entirely new light into the mystery behind how changes in the beta cell may play a role in the earliest stages of T1D, and adds a new perspective to our understanding how T1D progresses, and how to prevent and treat the disease. 

More about the study, published in the March 22 issue of the journal Diabetes, the researchers, led by Sarah Tersey, Ph.D., assistant research professor of pediatrics, and Raghavendra Mirmira, M.D., Ph.D., professor of pediatrics and medicine at the Indiana University School of Medicine is online here: 

http://www.eurekalert.org/pub_releases/2012-03/jdrf-rfb032212.php 

Type 2 Autoimmune - Say What?

A Standford / U of Toronto study suggest that type 2 may have roots in an autoimmune process.

That link is http://med.stanford.edu/ism/2011/april/engleman.html and in part it says:

Nearly all type-2 diabetes drugs marketed today are designed to control a patient’s high blood sugar levels — a symptom of the body’s inability to respond properly to insulin. However, the researchers found that anti-CD20, which targets and eliminates mature B cells, could completely head off the development of type-2 diabetes in laboratory mice prone to the disorder and restore their blood sugar levels to normal.

As I understand this release, and let me be clear - I don't understand it, T cells and B cells inflame fatty tissues. This results in fat cells growing so rapidly that they exceed their blood supply and begin to die. To clean up the dieing cells the immune system creates macrophages. This process of inflammation, dieing and clean up inhibits the remaining fat cells ability to respond to insulin.

The significance is that this suggest a new process for type 2, an autoimmune process. The study suggest treatments based on this autoimmune reaction that are new ways of addressing type 2, specifically an antibody called anti-CD20. This antibody is already approved for use in humans to treat some blood cancers and autoimmune diseases.

Daniel Winer, DM of Stanford says, “We are in the process of redefining one of the most common diseases in America as an autoimmune disease, rather than a purely metabolic disease.”

As regular readers may have guessed,  mice were involved in the studies. How this translates to humans is an open issue. This statement warented it own paragraph in the relaease: "Despite the treatment’s effectiveness in mice, the researchers caution against assuming rituximab will work in humans with established type-2 diabetes."

More Studies are require.

YDMV.