Pathogenesis of Insulin Resistance in Skeletal Muscle
By Muhammad Abdul-Ghani, Ralph DeFronzo. Journal of Biomedicine and Biotechnology, 2010
668 citations recorded by the source corpus.
Insulin resistance in skeletal muscle is manifested by decreased insulin-stimulated glucose uptake and results from impaired insulin signaling and multiple post-receptor intracellular defects including impaired glucose transport, glucose phosphorylation, and reduced glucose oxidation and glycogen synthesis. Insulin resistance is a core defect in type 2 diabetes, it is also associated with obesity and the metabolic syndrome. Dysregulation of fatty acid metabolism plays a pivotal role in the pathogenesis of insulin resistance in skeletal muscle. Recent studies have reported a mitochondrial defect in oxidative phosphorylation in skeletal muscle in variety of insulin resistant states. In this review, we summarize the cellular and molecular defects that contribute to the development of insulin resistance in skeletal muscle.
Subfields: Molecular Biology, Physiology
View Paper: https://www.semanticscholar.org/paper/ae0836fd0213314956d83d1c268fc71c268be37f
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Citations in the corpus
- Demonstrated brain insulin resistance in Alzheimer's disease patients is associated with IGF-1 resistance, IRS-1 dysregulation, and cognitive decline. (2012, neutral): “As diagrammed in Supplemental Figure 1 (supplemental material available online with this article; doi:10.1172/JCI59903DS1), the upstream portion of that pathway uses the following activation sequence: IR → IRS-1/2 → PI3K → Akt (the last of which is also referred to as PKB) (41–44).”
- Pathophysiology of Type 2 Diabetes Mellitus (2020, background): “Thus, mutations in any of the main phosphorylation sites can impair INSR tyrosine kinase activity, thereby impairing insulin action on skeletal muscle [161].”