New York, NY, August 7, 2012--When JDRF-funded research teams from two separate universities met three years ago, they learned that they were on similar paths in their attempt to discover the link connecting beta cell stress with inflammation and beta cell death in type 1 diabetes (T1D). Rather than racing to be the first to reveal preliminary findings, however, the teams from the University of California, San Francisco (UCSF), and Washington University School of Medicine in St. Louis decided that their cooperation would provide a more comprehensive understanding of the basis of the disease and would thus be more beneficial to diabetes research. The two labs moved forward with their separate studies, communicating regularly to exchange new findings. In the end, both teams had independently discovered how the beta cell protein TXNIP links cell stress with inflammation and cell death. Both studies will be published in the August 8th print edition of Cell Metabolism, and are available online (www.cell.com) from today.
"Inflammation is a major factor in the death of insulin-producing beta cells during the progression of type 1 diabetes; however, the mechanisms initiating inflammation in type 1 diabetes were elusive," said Fumihiko Urano, M.D., Ph.D., primary investigator of the study at Washington University. "We discovered that beta cell stress plays an important role in the initiation of inflammation through TXNIP."
Shortly after I was diagnosed in 1984 I visited UCSF and they said my type 1 was probably caused by strept throat I got about 9 months before that was so severe that I was hospitalized for about a week. They said it was known that type 1 was typically triggered by a stress which could be a virus, some type of infection, or high stress like a family member dying. The stress on the body somehow triggers the immune system to go haywire. Not sure if it is true, but that is what they said almost 30 years ago at UCSF.
These research results on the role of inflammation in diabetes gels well with my experience at a T2 of a quick and striking drop in my insulin requirements when I changed to an anti-inflammatory, high nutrient diet and cut back on inflammatory substances.