Mitochondrial dysfunction in type 2 diabetes and obesity.
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.
Højlund
Kurt
K
Diabetes Research Center, Department of Endocrinology, Odense University Hospital, Kloevervaenget 6, 3 DK-5000 Odense C, Denmark. k.hojlund@dadlnet.dk
Mogensen
Martin
M
Sahlin
Kent
K
Beck-Nielsen
Henning
H
D003924:Diabetes Mellitus, Type 2 / Q000378:metabolism*; D006801:Humans; D007333:Insulin Resistance; D008928:Mitochondria / Q000502:physiology*; D009765:Obesity / Q000378:metabolism*; D001678:Organelle Biogenesis; D010084:Oxidation-Reduction; D040901:Proteomics