Syndicate content

Archive - Jan 28, 2015

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.

Easter Island Decline Began Prior to Arrival of Europeans

Long before the Europeans arrived on Easter Island in 1722, the native Polynesian culture known as Rapa Nui showed signs of demographic decline. However, the catalyst has long been debated in the scientific community. Was environmental degradation the cause, or could a political revolution or an epidemic of disease be to blame? A new study by a group of international researchers, including Universty of Caifornia (UC) UC Santa Barbara’s Dr. Oliver Chadwick, offers a different explanation and helps to clarify the chronological framework. The investigators expected to find that changes coincided with the arrival of the Europeans, but their work shows instead that the demise of the Rapa Nui culture began prior to that. Their findings are published in the January 27, 2015 issue of PNAS. "In the current Easter Island debate, one side says the Rapa Nui decimated their environment and killed themselves off," said Dr. Chadwick, a professor in UC Santa Barbara's Department of Geography and the Environmental Studies Program. "The other side says it had nothing to do with cultural behavior, that it was the Europeans who brought disease that killed the Rapa Nui. Our results show that there is some of both going on, but the important point is that we show evidence of some communities being abandoned prior to European contact." Dr. Chadwick joined archaeologists Dr. Christopher Stevenson of Virginia Commonwealth University, Dr. Cedric Puleston of UC Davis and Dr. Thegn Ladefoged of the University of Auckland, New Zealand in examining six agriculture sites used by the island's statue-building inhabitants. The research focused mainly on the three sites for which the scientists had information on climate, soil chemistry, and land use trends, as determined by an analysis of obsidian spear points.