Mitochondrial dysfunction in type 2 diabetes and obesity
- PMID: 18775360
- DOI: 10.1016/j.ecl.2008.06.006
Mitochondrial dysfunction in type 2 diabetes and obesity
Abstract
Insulin resistance in skeletal muscle is a major hallmark of type 2 diabetes mellitus (T2D) and obesity that is characterized by impaired insulin-mediated glucose transport and glycogen synthesis and by increased intramyocellular content of lipid metabolites. Several studies have provided evidence for mitochondrial dysfunction in skeletal muscle of type 2 diabetic and prediabetic subjects, primarily due to a lower content of mitochondria (mitochondrial biogenesis) and possibly to a reduced functional capacity per mitochondrion. This article discusses the latest advances in the understanding of the molecular mechanisms underlying insulin resistance in human skeletal muscle in T2D and obesity, with a focus on possible links between insulin resistance and mitochondrial dysfunction.
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