The discovery could mean that new treatments for the prevention of cell death-β or restoration which have already lost, Kathrin Mädler and colleagues report in the February 4th issue of Cell Metabolism, a publication of Cell press. Inflammatory factor discovered, they call for CXCL10 can also be a warning signal for the beginning or before the disease, she said.
“In the past, the idea that insulin resistance is a diabetic, but the loss of β-comes in two cells of type 1 and type 2 diabetes,” said Madl, recalling that those who are insulin resistance, to 10-20 per cent go to type 2 diabetes by a disruption of β cells. “We found inflammation markers for both types of diabetes. If we can protect the cells of CXCL10 expression, we can prevent the decrease in β cell mass, and therefore the disease. ”
Type 1 diabetes is diagnosed, usually in children and young adults, and it follows from the inability to produce insulin. The most common type 2 diabetes is usually later in life, if the body is not enough insulin or does not develop on the hormone.
In case of type 1 diabetes, β cells are destroyed by the immune system and production of high concentrations of inflammatory signals. While scientists had swum a lot of ideas, exactly what causes loss of β cell in type 2 diabetes is a matter of debate.
Mädler team have inflammatory factors may play an important role too. In fact, inflammatory markers are obesity, insulin resistance and diabetes, they. Previous studies have also shown that low grade inflammation and activation of the innate immune system, instead of the first line of defense – may lead to errors in the beta-cells in type II diabetes.
You have now established that inflammatory factors CXCL10 (also known as interferon-gamma inducible protein-10 or IP 10) is an important factor in β-cell destruction. They found that the hormone-producing cells isolated from patients with type 2 diabetes sekretieren CXCL10 and more than 30 times the amount of CXCL10 personal form of RNA, such as cells of patients without diabetes.
Pancreas sections of overweight people without type 1 diabetes or type 2 diabetes showed CXCL10 in β-cells, they found. In addition, treatment of the isolation of human pancreatic cells with CXCL10 decreased β cell and affects the profitability of production and secretion of insulin. It follows the impact of CXCL10 way to a knowledge of the innate immune system, the protein as the Toll-like receptor 4 (TLR4).
The new data suggest a potential mechanism for the conversion of β cells “programmed distribution of their cells, the researchers conclude.” To prevent such a development, the objectives of the anti-inflammatory TLR4 signal is of paramount importance for the rescue of the β cells of the inflammation induced by self-destruction and [to] preserve β cell function and the earth. ”
Researchers are Fabienne T. Schulthess, University of California, Los Angeles, Los Angeles, CA, University of Bremen, Bremen, Germany; Paroni Federico, University of Bremen, Bremen, Germany; Nadine P. Sauter, University of California, Los Angeles, Los Angeles, CA; Luan Shu, University of California, Los Angeles, Los Angeles, CA, University of Bremen, Bremen, Germany; Ribaux Pascale, University Medical Center, Geneva, Switzerland; Leena Haataja , University of California, Los Angeles, Los Angeles, CA, Robert M. Strieter, University of Virginia School of Medicine, Charlottesville, VA; Jose Oberholzer, University of Illinois at Chicago, Chicago, IL, Charles C. King, University of California, San Diego, La Jolla, CA and Kathrin Mädler, University of California, Los Angeles, Los Angeles, CA, University of Bremen, Bremen, Germany
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