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All rights reserved. http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Large Corpus Document http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RAuA0lFVBfpgz8eObWO9TNkqvm0-oybz_yNU2pb3UR0NA#_4 http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/version 1.4 http://www.tkuhn.ch/bel2nanopub/RAuA0lFVBfpgz8eObWO9TNkqvm0-oybz_yNU2pb3UR0NA#_3 http://www.w3.org/ns/prov#value Insulin can also influence glucose metabolism indirectly by changes in free fatty acids generated from visceral fat, the so called 'single gateway' hypothesis64. Because visceral fat is less sensitive to insulin than subcutaneous fat, even after a meal there is little suppression of lipolysis by the hormone in this fat depot. The resulting direct flux of fatty acids derived from these fat cells through the portal vein to the liver can stimulate glucose production, thus providing a signal for both insulin action and insulin resistance in the liver It [insulin] inhibits the transcription of the gene encoding phosphoenolpyruvate carboxylase, the rate-limiting step in gluconeogenesis66. 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