Abstract
Insulin resistance is a feature of a number of clinical disorders, including type 2 diabetes/glucose intolerance, obesity, dyslipidaemia and hypertension clustering in the so-called metabolic syndrome. Insulin resistance in skeletal muscle manifests itself primarily as a reduction in insulin-stimulated glycogen synthesis due to reduced glucose transport. Ectopic lipid accumulation plays an important role in inducing insulin resistance. Multiple defects in insulin signalling are responsible for impaired glucose metabolism in target tissues of subjects with features of insulin resistance. Inflammatory molecules and lipid metabolites inhibit insulin signalling by stimulating a number of different serine kinases which are responsible for serine phosphorylation of Insulin Receptor Substrate-1 (IRS-1).
MeSH terms
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Cytokines / physiology
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Fatty Acids / pharmacology
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Glucose / metabolism*
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Glucose Transporter Type 4 / physiology
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Glycogen
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Humans
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Insulin / physiology
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Insulin Resistance / physiology*
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Muscles / metabolism
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Phosphatidylinositol 3-Kinases / physiology
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Phosphoric Diester Hydrolases / physiology
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Protein Kinase C / physiology
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Protein Tyrosine Phosphatase, Non-Receptor Type 1
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Protein Tyrosine Phosphatases / physiology
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Proto-Oncogene Proteins c-akt / physiology
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Pyrophosphatases / physiology
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Receptor, Insulin / genetics
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Signal Transduction / drug effects
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Signal Transduction / physiology
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Somatomedins / physiology
Substances
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Cytokines
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Fatty Acids
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Glucose Transporter Type 4
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Insulin
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Somatomedins
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Glycogen
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Phosphatidylinositol 3-Kinases
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Receptor, Insulin
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Proto-Oncogene Proteins c-akt
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protein kinase C zeta
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Protein Kinase C
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PTPN1 protein, human
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Protein Tyrosine Phosphatase, Non-Receptor Type 1
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Protein Tyrosine Phosphatases
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Phosphoric Diester Hydrolases
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ectonucleotide pyrophosphatase phosphodiesterase 1
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Pyrophosphatases
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Glucose