A new study conducted by the University of Cambridge has answered a question long posed by diabetes researchers: does insulin resistance cause mitochondrial damage or does mitochondrial damage cause insulin resistance?
The answer: insulin resistance comes first.
Coming to this conclusion was not easy because most people with type 2 diabetes exhibit both symptoms of insulin resistance and mitochondrial damage making it hard to tell which came first, or affecting the other, or, if something completely different caused both problems.
For their study, which was published in the Journal of Clinical Investigation, they examined individuals born with genetic defects in their insulin receptors. These receptors are responsible for mediating the effects of insulin, and a dysfunction can leave individuals resistant to the hormone, mimicking the symptoms of type 2 diabetes.
According to EndocrineWeb.com:
The researchers tested phosphocreatine recovery time in these individuals after they exercised. This is considered to be a measure of skeletal muscle mitochondrial function in the body. Compared to healthy individuals, those with insulin receptor mutations had significantly slower recovery times.
These results indicated to the investigation team that insulin signaling dysfunction and insulin resistance are the root cause of mitochondrial dysfunctions. These findings likely explain why many individuals with type 2 diabetes also experience the damage to these organelles.
Upon further examination, the researchers found that insulin-resistant participants had much faster sleeping metabolic rates. They speculated that this could be because impaired mitochondrial function may necessitate increased nutrient oxidation to maintain energy levels.
Mitochondrial dysfunction has its own set of health concerns. It can lead to chronic fatigue syndrome, muscle weakness, hearing problems and loss of vision and is difficult to treat.
Source: Insulin resistance precedes mitochondrial dysfunction in type 2 diabetics, study finds. EndocrineWeb.com, May 10, 2011.