About: Insulin Resistance Pathway     Goto   Sponge   NotDistinct   Permalink

An Entity of Type : owl:Class, within Data Space : linked.opendata.cz:8890 associated with source document(s)

AttributesValues
rdf:type
rdfs:label
  • Insulin Resistance Pathway
rdfs:subClassOf
Semantic_Type
  • Functional Concept
Preferred_Name
  • Insulin Resistance Pathway
UMLS_CUI
  • C1512803
BioCarta_ID
  • h_leptinPathway
ALT_DEFINITION
  • The insulin resistance of type II diabetes appears to be caused in part by the presence of high levels of lipids in cells such as skeletal muscle where this would not normally be found. The presence of excess lipid stores in skeletal muscle cells interferes with energy metabolism, impairing glucose oxidation and insulin response. Skeletal muscle is one of the primary glucose-consuming tissues, giving it a central role in insulin resistance. The increased risk of diabetes associated with obesity may be caused by increased lipid deposits in skeletal muscle and liver, creating insulin resistance. Leptin is a peptide hormone secreted by adipose tissue that has been associated with many processes. One of the target tissues of leptin is the hypothalamus where it can act to regulate feeding behavior and metabolism. Another leptin target is skeletal muscle. Activation of leptin signaling in skeletal muscle activates the AMP-activated protein kinase (AMP-kinase), known to play a key role in signaling in response to nutrients throughout evolution. AMPK phosphorylates and inactivates the enzyme ACC, acetyl-CoA carboxylase. ACC catalyzes the production of malonyl-CoA from acetyl-CoA. Malonyl-CoA in turn is an inhibitor of the import of fatty acids into mitochondria by carnitine palmitoyltransferase I for oxidation and energy production. In the presence of leptin, AMPK is activated, ACC is inhibited, and malonyl-CoA levels fall, increasing the oxidation of fatty acids and reducing the lipid content of cells. The reduced lipid content in skeletal muscle allows insulin signaling and glucose consumption to return to their normal levels, reducing insulin resistance.BIOCARTA
Legacy_Concept_Name
  • Insulin_Resistance_Pathway
FULL_SYN
  • Reversal of Insulin Resistance by LeptinPTBIOCARTA
  • Insulin Resistance PathwayPTNCI
code
  • C39139
is someValuesFrom of
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