Every cell in our bodies contains bacteria-sized powerhouses called mitochondria (seen as ovals in photo), where sugar combines with oxygen to produce adenosine triphosphate (ATP), the fuel for cells’ most important functions.
Insulin, which escorts sugar into cells, is a crucial player in this process. In type 2 diabetes, which affects 171 million people worldwide, cells become resistant to insulin and cellular energy production plummets.
A study in the September issue of PLoS Medicine led by Kitt F. Petersen, M.D., associate professor of medicine, suggests that insulin resistance results from an inherited flaw in mitochondrial function.
Petersen’s team used magnetic resonance spectroscopy to zoom in on the effects of insulin in muscle cells of children whose parents have type 2 diabetes and in a control group. They found a striking difference: insulin spiked ATP production by mitochondria in the control group’s muscle cells by 90 percent, but insulin-resistant offspring of parents with type 2 diabetes had only a 5 percent increase.
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