Researchers at Children's Hospital Boston have identified a new strategy for treating type 2 diabetes, identifying a cellular pathway that fails when people become obese.
By re-activating this pathway artificially, they were able to normalize blood glucose levels in severely obese and diabetic mice. Their findings will be published online by Nature Medicine on March 28.
Epidemiologists have long known that obesity contributes to type 2 diabetes. In previous work, researcher Umut Ozcan, MD, in Division of Endocrinology at Children's, showed that the brain, liver and fat cells of obese mice have increased stress in the endoplasmic reticulum (ER), a structure in the cell where proteins are assembled, folded into their proper shapes, and dispatched to do jobs for the cell. In the presence of obesity, the ER is overwhelmed and its operations break down.
This so-called "ER stress" activates a cascade of events that suppress the body's response to insulin, and is a key link between obesity and type 2 diabetes.
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