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Archive - Jul 8, 2009


A Molecular Link Between Obesity and Type 2 Diabetes Discovered

Although obesity is a major risk factor for type 2 diabetes, the factors linking these disorders are not well defined. Now, scientists at Monash University in Australia, and collaborating institutions, have obtained evidence for a molecular link between the two conditions. In a mouse model, the researchers have shown that a novel protein (pigment epithelium-derived factor or PEDF) released by fat cells triggers a chain of events and interactions that lead to the development of type 2 diabetes. "When PEDF is released into the bloodstream, it causes the muscle and liver to become desensitized to insulin. The pancreas then produces more insulin to counteract these negative effects," said Dr. Matthew Watt, senior author of the study. “This insulin release causes the pancreas to become overworked, eventually slowing or stopping insulin release from the pancreas, leading to type 2 diabetes. Our research was able to show that increasing PEDF not only causes type 2 diabetes-like complications but that blocking PEDF reverses these effects. The body again returned to being insulin-sensitive and therefore did not need excess insulin to remain regulated," Dr. Watt continued. "Until now scientists knew there was a very clear pattern and had strong suspicions that a link existed between the two conditions, but our understanding of the chain of events that are caused by the release of PEDF shows a causal link," Dr. Watt said. The results of this work were published in the July 8 issue of Cell Metabolism. [Press release] [Cell Metabolism abstract]

Easter Island Compound Extends Lifespan of Older Mice

In a multi-center study, scientists have shown that a compound first discovered in the soil of Easter Island can extend the lifespan of older mice. The compound is rapamycin, named from the Polynesian for the island, Rapa Nui. Discovered in the 1970s, rapamycin was first noted for its anti-fungal properties and later was used to prevent organ rejection in transplant patients. It is also used in stents, which are implanted in patients during angioplasty to keep coronary arteries open. It is in clinical trials for the treatment of cancer. In the current work, when rapamycin was added to the diets of older, genetically diverse mice (at an age equivalent to 60 years in humans), it extended lifespan by 28 to 38 percent. In human terms, this would be greater than the predicted increase in extra years of life if cancer and heart disease were both cured and prevented. "I've been in aging research for 35 years and there have been many so-called 'anti-aging' interventions over those years that were never successful," said Dr. Arlan G. Richardson, director of the Barshop Institute for Longevity and Aging Studies, and not involved in the study. "I never thought we would find an anti-aging pill for people in my lifetime; however, rapamycin shows a great deal of promise to do just that." "We believe this is the first convincing evidence that the aging process can be slowed and lifespan can be extended by a drug therapy starting at an advanced age," said Dr. Randy Strong, a lead author of the study. Aging researchers currently acknowledge only two life-extending interventions in mammals: calorie restriction and genetic manipulation. Rapamycin appears to partially shut down the same molecular pathway as restricting food intake or reducing growth factors.