Abstract
As a major site of glucose uptake following a meal, skeletal muscle has an important role in whole-body glucose metabolism. Evidence in humans and animal models of insulin resistance and type 2 diabetes suggests that alterations in mitochondrial characteristics accompany the development of skeletal muscle insulin resistance. However, it is unclear whether changes in mitochondrial content, respiratory function, or substrate oxidation are central to the development of insulin resistance or occur in response to insulin resistance. Thus, this review will aim to evaluate the apparent conflicting information placing mitochondria as a key organelle in the development of insulin resistance in skeletal muscle.
Highlights
In response to increased blood glucose levels, such as after a meal, insulin is released by the β-cells of the pancreas
A lower skeletal muscle mitochondrial content has typically been observed in people with insulin resistance and type 2 diabetes
Lower skeletal muscle mitochondrial content is not likely to be directly responsible for the development of insulin resistance and type 2 diabetes (T2D)
Summary
In response to increased blood glucose levels, such as after a meal, insulin is released by the β-cells of the pancreas. Many studies have shown that people with T2D, a family history of T2D, obesity, and/or insulin resistance, have decreased skeletal muscle mitochondrial respiratory function and/or content [5,6,7,8,9]. Humans with insulin resistance and T2D have a decreased expression of genes encoding key enzymes involved in fatty acid oxidation and the tricarboxylic acid (TCA) cycle, as well as components of the respiratory chain [10]; a lower abundance of mitochondrial proteins has been reported [11]. There is considerable conflict in the literature and whether alterations in skeletal muscle mitochondria are a cause or consequence of insulin resistance is yet to be established [12]
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