Researchers Relate Mitochondria Activity to Type 2 Diabetes

insulin.jpgInsulin resistance, the predecessor to Type 2 Diabetes, relates to the ineffectiveness of the insulin hormone to transfer glucose into the body’s cells to be used as fuel. In particular, insulin binds to a spot on the cell surface called a receptor. Likened to a lock and key, insulin is the key that opens up the lock (receptor) so that glucose can pass through the door into the cell. Using this analogy in Type 1 diabetes, the keys have been stolen (no insulin is made by the pancreas). In Type 2, the door won’t open fully even with the right key (insulin resistance). [Source: FDA]
Although there has been a lot of emphasis on lifestyle and nutritional risk factors which influence the onset of the disease, fundamental questions remain regarding what actually causes Type 2 diabetes. For example, why do some individuals, who are do not have lifestyle risk factors, become diabetic? And, what causes insulin to be ineffective?
Physiologist Gerald Shulman and his colleagues at Yale University took on these questions in a study of 20-year-olds whose parents are diabetic. Despite being young, healthy and lean, all of the test subjects had high levels of insulin resistance:

Insulin resistance is often referred to as “pre-diabetes” because it’s the first sign that the body is not processing sugar properly.
After eating a meal, the digestive system breaks most food down into units of glucose, a simple sugar that is one of the basic energy sources for the body. Insulin is a hormone made by the pancreas, which triggers cells to absorb the glucose and use it. Once inside the cell, small energy factories called mitochondria convert the glucose sugar into a chemical called ATP. ATP powers every cellular and bodily function, from thinking to moving. When someone is insulin resistant, his or her cells aren’t able to absorb sugar from the bloodstream to make ATP, which leaves the cells starving for energy even though it’s right there just outside the cell wall.

Interestingly, although the study participants were lean, they had more fat inside their muscle cells than is typical.

Shulman says, “Fat inside the muscle cell causes insulin resistance; so the real question becomes, ‘Why is the fat building up?’ … So it became a question of, are there defects in the fat cells in the body, releasing more fat to liver and muscle, causing the buildup? Or are there defects in the mitochondria… the factories in all the cells of our body that produce energy?”


Cellular analysis revealed that compared to non-diabetic volunteers, the insulin-resistant group had much less mitochondrial activity, leading to the fat building up inside the cells. Shulman’s team has also determined that the lower mitochondrial activity in these insulin-resistant patients is actually due to the presence of fewer mitochondria.
This is all very interesting, but where the research becomes exciting is the potential for unlocking new prevention and treatment options from a better understanding of the underlying cause and disease mechanisms. Until the realization of these, however, Shulman recommends (to no ones surprise): proper diet and exercise.
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  1. Researchers Relate Mitochondria Activity to Type 2 Diabetes

    Insulin resistance, the predecessor to Type 2 Diabetes, relates to the ineffectiveness of the insulin hormone to transfer glucose into the body’s cells to be used as fuel. In particular, insulin binds to a spot on the cell surface called a receptor.