L-glutamine supplementation induces insulin resistance in adipose tissue and improves insulin signalling in liver and muscle of rats with diet-induced obesity

dc.creatorPrada, PO
dc.creatorHirabara, SM
dc.creatorde Souza, CT
dc.creatorSchenka, AA
dc.creatorZecchin, HG
dc.creatorVassallo, J
dc.creatorVelloso, LA
dc.creatorCarneiro, E
dc.creatorCarvalheira, JBC
dc.creatorCuri, R
dc.creatorSaad, MJ
dc.date2007
dc.dateSEP
dc.date2014-11-17T16:40:20Z
dc.date2015-11-26T17:40:38Z
dc.date2014-11-17T16:40:20Z
dc.date2015-11-26T17:40:38Z
dc.date.accessioned2018-03-29T00:22:20Z
dc.date.available2018-03-29T00:22:20Z
dc.identifierDiabetologia. Springer, v. 50, n. 9, n. 1949, n. 1959, 2007.
dc.identifier0012-186X
dc.identifierWOS:000248771800020
dc.identifier10.1007/s00125-007-0723-z
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/80890
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/80890
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/80890
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1286781
dc.descriptionAims/hypothesis Diet-induced obesity (DIO) is associated with insulin resistance in liver and muscle, but not in adipose tissue. Mice with fat-specific disruption of the gene encoding the insulin receptor are protected against DIO and glucose intolerance. In cell culture, glutamine induces insulin resistance in adipocytes, but has no effect in muscle cells. We investigated whether supplementation of a high-fat diet with glutamine induces insulin resistance in adipose tissue in the rat, improving insulin sensitivity in the whole animal. Materials and methods Male Wistar rats received standard rodent chow or a high-fat diet (HF) or an HF supplemented with alanine or glutamine (HFGln) for 2 months. Light microscopy and morphometry, oxygen consumption, hyperinsulinaemic-euglycaemic clamp and immunoprecipitation/immunoblotting were performed. Results HFGln rats showed reductions in adipose mass and adipocyte size, a decrease in the activity of the insulin-induced IRS-phosphatidylinositol 3-kinase (PI3-K)-protein kinase B-forkhead transcription factor box 01 pathway in adipose tissue, and an increase in adiponectin levels. These results were associated with increases in insulin-stimulated glucose uptake in skeletal muscle and insulin-induced suppression of hepatic glucose output, and were accompanied by an increase in the activity of the insulin-induced IRS-PI3-K-Akt pathway in these tissues. In parallel, there were decreases in TNF alpha and IL-6 levels and reductions in c-jun N-terminal kinase (JNK), I kappa B kinase subunit beta (IKK beta) and mammalian target of rapamycin (mTOR) activity in the liver, muscle and adipose tissue. There was also an increase in oxygen consumption and a decrease in the respiratory exchange rate in HFGln rats. Conclusions/interpretation Glutamine supplementation induces insulin resistance in adipose tissue, and this is accompanied by an increase in the activity of the hexosamine pathway. It also reduces adipose mass, consequently attenuating insulin resistance and activation of JNK and IKK beta, while improving insulin signalling in liver and muscle.
dc.description50
dc.description9
dc.description1949
dc.description1959
dc.languageen
dc.publisherSpringer
dc.publisherNew York
dc.publisherEUA
dc.relationDiabetologia
dc.relationDiabetologia
dc.rightsfechado
dc.rightshttp://www.springer.com/open+access/authors+rights?SGWID=0-176704-12-683201-0
dc.sourceWeb of Science
dc.subjectakt
dc.subjectglutamine
dc.subjecthigh-fat diet
dc.subjectinsulin resistance
dc.subjectinsulin signalling
dc.subjectphosphatidylinositol 3-kinase
dc.subjectobesity
dc.subjectPI-3K
dc.subjectAmino-acid-metabolism
dc.subjectReceptor Substrate-1
dc.subjectIn-vivo
dc.subjectHexosamine Pathway
dc.subjectSkeletal-muscle
dc.subjectProtein-kinase
dc.subjectSoleus Muscle
dc.subjectGlucose
dc.subjectMice
dc.subjectPhosphorylation
dc.titleL-glutamine supplementation induces insulin resistance in adipose tissue and improves insulin signalling in liver and muscle of rats with diet-induced obesity
dc.typeArtículos de revistas


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