Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/10001
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dc.contributor.authorProietto, Josephen
dc.date.accessioned2015-05-15T23:18:37Z
dc.date.available2015-05-15T23:18:37Z
dc.date.issued2005-10-03en
dc.identifier.citationHepatology Research : the Official Journal of the Japan Society of Hepatology 2005; 33(2): 87-91en
dc.identifier.govdoc16203173en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/10001en
dc.description.abstractInsulin resistance, the impaired action of insulin, has been linked to many important consequences, including Type 2 diabetes, hypertension, dyslipidemia, acanthosis nigricans and polycystic ovarian syndrome. Although there are some genetic causes for insulin resistance, the most common cause is an excess of nutrition a condition called "Nutrient Toxicity". Both excess glucose and excess fat can cause insulin resistance in muscle and fat tissues and excess fat can cause insulin resistance in the liver. High fat feeding and fat infusion rapidly lead to the development of insulin resistance caused by impairment in glucose transport. Other studies have shown defects in insulin signaling possibly secondary to activation of Protein Kinase C resulting from the accumulation of active fatty acyl CoA's. Glucose toxicity has been studied both in vivo and in vitro. In vivo it has been shown that rats over-expressing the gluconeogenic enzyme Phosphoenol Pyruvate Carboxykinase (PEPCK) develop insulin resistance in fat and muscle tissues and some features of the metabolic syndrome including mild obesity and dyslipidemia. Excess glucose entry in fat cells results in increased flux through the hexosamine biosynthesis pathway leading to activation of protein kinase C and impairment of glucose transport. Obesity resulting from excess nutrient intake can also cause insulin resistance by an increase in the production of agents that impair insulin action such as TNFalpha and resistin and a decrease in the production of an insulin sensitizing compound adiponectin. Both glucose and free fatty acids acutely stimulate insulin secretion but chronic exposure to high levels of either nutrient leads to impairment of beta cell function. The combination of insulin resistance and beta cell failure leads to diabetes. Nutrient toxicity is thus the driving cause of the diabetes epidemic that is being recorded around the world.en
dc.language.isoenen
dc.titleMechanisms of insulin resistance caused by nutrient toxicity.en
dc.typeJournal Articleen
dc.identifier.journaltitleHepatology research : the official journal of the Japan Society of Hepatologyen
dc.identifier.affiliationUniversity of Melbourne, Department of Medicine, Repatriation Hospital, Austin Health, Heidelberg Heights, Melbourne, Vic. 3081, Australiaen
dc.identifier.doi10.1016/j.hepres.2005.09.010en
dc.description.pages87-91en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/16203173en
dc.type.austinJournal Articleen
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.fulltextNo Fulltext-
item.cerifentitytypePublications-
item.grantfulltextnone-
item.languageiso639-1en-
item.openairetypeJournal Article-
crisitem.author.deptMedicine (University of Melbourne)-
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