Insulin resistance precedes mitochondrial dysfunction in type 2 diabetics, study finds

Insulin resistance, which is common in individuals with type 2 diabetes, may result from dysfunctions in the mitochondria, according to a new study from researchers at the University of Cambridge. The findings help answer an enduring mystery that has perplexed diabetes investigators for years.

It has long been known that individuals with type 2 diabetes often suffer from dysfunctions in their mitochondria, which are organelles contained within cells that produce energy. However, it was not known whether these mitochondrial irregularities were the cause of insulin resistance and diabetes, or whether a single preexisting difference accounted for both insulin resistance and impaired mitochondrial function.

Studying these conditions is difficult, because most people who exhibit one of the symptoms also has the other. Therefore, it is difficult to determine which came first. However, the researchers came up with a unique solution to this problem.



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.



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.

The findings help answer a question that had long plagued diabetes experts. By showing that insulin resistance is in fact the cause of mitochondrial dysfunction rather than the other way around, the results could provide direction to future researchers who are looking to solve the health consequences that can result from either condition.

Aside from the risk of health complications associated with type 2 diabetes, mitochondrial dysfunction can lead to muscle weakness, hearing problems and loss of vision. It can be difficult to treat.
 
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