dc.creatorBonfleur, Maria Lúcia
dc.creatorBorck, Patrícia Cristine
dc.creatorRibeiro, Rosane Aparecida
dc.creatorCaetano, Luiz Carlos
dc.creatorSoares, Gabriela Moreira
dc.creatorCarneiro, Everardo Magalhães
dc.creatorBalbo, Sandra Lucinei
dc.date2015-Aug
dc.date2016-05-23T19:42:10Z
dc.date2016-05-23T19:42:10Z
dc.date.accessioned2018-03-29T01:29:30Z
dc.date.available2018-03-29T01:29:30Z
dc.identifierLife Sciences. v. 135, p. 15-21, 2015-Aug.
dc.identifier1879-0631
dc.identifier10.1016/j.lfs.2015.05.019
dc.identifierhttp://www.ncbi.nlm.nih.gov/pubmed/26092479
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/235690
dc.identifier26092479
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1303933
dc.descriptionFat deposition in the liver, which leads to nonalcoholic fatty liver disease is associated with obesity. Taurine (Tau) regulates lipid metabolism, representing a possible nutraceutical agent against obesity and its comorbidities. Here, we investigated whether Tau supplementation prevents hepatic lipid accumulation by regulation of the main hepatic genes involved in de novo lipogenesis and β-oxidation. Male rats received subcutaneous injections of monosodium glutamate (MSG; 4 mg/kg body weight/day) or saline (control group, CTL) during the first 5 days of life. From 21 to 120 days of age, half of each of the MSG and CTL groups received 2.5% Tau in drinking water (CTau and MTau). MSG-treated rats were normoglycemic, hypertriglyceridemic and insulin resistant (IR). MSG rats also exhibited massive obesity and higher hepatic triglyceride (TG) content. This effect was associated with enhanced gene expression of fatty acid synthase (FASN), but reduced carbohydrate response element-binding protein (ChREBP), microsomal TG transfer protein (MTP) and carnitine palmitoyltransferase (CPT)-1a mRNAs in MSG livers. Tau supplementation decreased whole body fat accumulation and serum TG levels, without altering IR. Tau also normalized hepatic TG content by enhancing ChREBP, MTP, peroxisome proliferator-activated receptor (PPAR)-α, ACO (acyl-CoA oxidase) and CPT-1a gene expressions. Therefore, increased hepatic TG deposition in MSG-obese rats is associated with an enhanced FASN, and reduced MTP and CPT-1a genes. Tau supplementation prevented obesity and hepatic TG deposition by upregulating MTP mRNA, ameliorating hepatic lipid efflux, and consequently enhancing PPAR-α which increases lipid oxidation through ACO and CPT-1a gene expressions.
dc.description135
dc.description15-21
dc.languageeng
dc.relationLife Sciences
dc.relationLife Sci.
dc.rightsembargo
dc.sourcePubMed
dc.subjectAcyl-coa Oxidase
dc.subjectCarnitine Palmitoyltransferase 1a
dc.subjectMsg-obesity
dc.subjectMicrosomal Tg Transfer Protein
dc.subjectMonosodium Glutamate (pubchem Cid: 16219392)
dc.subjectPeroxisome Proliferator-activated Receptor α
dc.subjectTaurine (pubchem Cid: 1123)
dc.subjectTaurine Supplementation
dc.titleImprovement In The Expression Of Hepatic Genes Involved In Fatty Acid Metabolism In Obese Rats Supplemented With Taurine.
dc.typeArtículos de revistas


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