Researchers come to new understanding of process that contributes to type 2 diabetes
A new study conducted by a group of researchers from the University of North Carolina may help clarify the connection between high levels of body fat, inflammation and insulin resistance, three factors that are known to increase type 2 diabetes risk but are still poorly understood by science.
The researchers reported in the journal Nature Immunology
that a diet rich in saturated fat, in addition to causing weight gain, activates certain cells of the immune system, instructing them to produce a protein called interleukin-1beta. This molecule is known to cause inflammation throughout the body.
This inflammation, in turn, affects the tissue of muscles, the liver and other organs, impairing their ability to react to insulin. This characteristic is one of the hallmarks of type 2 diabetes. Jenny Ting, who led the research, said that the findings help explain some of the aspects of type 2 diabetes that were thought to be connected, but which lacked evidence to support a link.
"The cellular path that mediates fatty acid metabolism is also the one that causes interleukin-1beta production," she said. "Interleukin-1beta then acts on tissues and organs such as the liver, muscle and fat (adipose) to turn off their response to insulin, making them insulin resistant. As a result, activation of this pathway by fatty acid can lead to insulin resistance and type 2 diabetes symptoms."
In addition to explaining a poorly understood set of processes that were known to increase type 2 diabetes risk, the findings also provide further evidence of the importance of choosing foods low in unhealthy saturated fats. The researchers found that unsaturated fats, like omega-3s, did not activate this process.