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dc.creatorGalgani F,José
dc.creatorDíaz B,Erik
dc.date2000-12-01
dc.date.accessioned2022-08-29T19:34:43Z
dc.date.available2022-08-29T19:34:43Z
dc.identifierhttp://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0034-98872000001200008
dc.identifier.urihttps://revistaschilenas.uchile.cl/handle/2250/206273
dc.descriptionFatty acids, obesity and insulin resistance relationship are discussed. In the last decades fatty acids (FA) have been implicated in the etiology of insulin resistance. Initially, this process was related to FA inhibitory effects on glucose uptake mediated by the FA oxidation metabolites. This mechanism known as the Randle cycle has been presently discarded based on recent evidence for FA effects on glucose metabolism. Now is known that cytosolic lipid content and FA molecular structure determines higher or lower storage and oxidation capacity. Another factor is given by Tumor Necrosis Factor-a, which is overexpressed in animal and human obesity, producing insulin signaling and glucose uptake inhibition. This paper discuss the role played by FA and obesity on insulin resistance, mainly in relation to FA effects on glucose metabolism in the liver, muscle and adipose tissues. In the obesity condition adipose tissue releases higher levels of free FA which in turn stimulates hepatic glucose production. Adipose tissue also, increase TNF-a secretion impairing glucose utilization and insulin signaling. In muscle, cytosolic lipid content activate a Protein Kinase that inhibits the insulin signaling and reduce GLUT-4 translocation. The study of cellular and metabolic changes associated to weight gain and its relationship with insulin resistance etiology are encouraged (Rev Méd Chile 2000; 128: 1354-60).
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dc.languagees
dc.publisherSociedad Médica de Santiago
dc.relation10.4067/S0034-98872000001200008
dc.rightsinfo:eu-repo/semantics/openAccess
dc.sourceRevista médica de Chile v.128 n.12 2000
dc.subjectFatty acids
dc.subjectGlucose
dc.subjectInsuline resistance
dc.subjectObesity
dc.titleObesidad y ácidos grasos en la etiología de la resistencia insulínica


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