Preventing Inflammation in Obese Fat Tissue Could Be Key to Preventing Type 2 Diabetes; Interleukin-33 Acts to Boost Treg Populations in Fat Tissue, Halting the Development of Type 2 diabetes, or Even Reversing the Disease in Preclinical Models Preventing

Preventing inflammation in obese fat tissue may hold the key to preventing or even reversing type 2 diabetes, new research has found. RScientists from Melbourne's Walter and Eliza Hall Institute in Australia, with colleagues from the RIKEN Institute in Japan, found they could “reverse” type 2 diabetes in laboratory models by dampening the inflammatory response in fat tissue. Dr. Ajith Vasanthakumar, Dr. Axel Kallies, and colleagues from the institutes discovered that specialized immune cells, called regulatory T cells (Tregs), played a key role in controlling inflammation in fat tissue and maintaining insulin sensitivity. The findings were published online on Jnuary 19, 2015 in Nature Immunology. More than 850,000 Australians are estimated to have type 2 diabetes, which is the most common type of diabetes, and its prevalence is rising. The disease is strongly linked with 'lifestyle' factors, such as being overweight or having high blood pressure. Long-term complications of type 2 diabetes include kidney, eye, and heart disease, and there is no cure. People with type 2 diabetes have reduced sensitivity to insulin, a hormone that normally triggers uptake of glucose by cells, and their cells no longer respond to insulin appropriately. This decrease in insulin sensitivity is thought to be a result of long-term, low-level inflammation of fat tissue in people who are obese. Dr. Vasanthakumar said Tregs acted as the guardians of the immune system, preventing the immune response from getting out-of-hand and attacking the body's own tissues. "When Treg numbers are reduced, inflammatory diseases such as diabetes and rheumatoid arthritis can occur," he said.
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