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Human Skeletal Muscle Glyoxalase‐1 Protein Expression is Attenuated with Type 2 Diabetes

Individuals with type 2 diabetes mellitus (T2DM) present with increased levels of advanced glycation endproducts (AGEs), which have been associated with progression and complications of the disease. AGEs are known to contribute to the disruption of insulin signaling in skeletal muscle and are primarily produced in vivo by the damaging glycolytic byproduct, methylglyoxal (MG). MG is effectively detoxified by the enzyme, glyoxalase‐1 (GLO1), whose protein expression has been previously shown to be inversely related to MG‐mediated protein‐damage and AGE formation. Despite the role of skeletal muscle insulin resistance in the pathogenesis of T2DM, GLO1 protein expression has not been fully elucidated in skeletal muscle. Additionally, the metabolic effects of insulin stimulation on GLO1 protein in human skeletal muscle has not been described.