dc.creatorStoppa, Graziela R
dc.creatorCesquini, Maristela
dc.creatorRoman, Erika A
dc.creatorPrada, Patrícia O
dc.creatorTorsoni, Adriana S
dc.creatorRomanatto, Talita
dc.creatorSaad, Mario J
dc.creatorVelloso, Licio A
dc.creatorTorsoni, Marcio A
dc.date2008-Jul
dc.date2015-11-27T13:12:49Z
dc.date2015-11-27T13:12:49Z
dc.date.accessioned2018-03-29T01:06:49Z
dc.date.available2018-03-29T01:06:49Z
dc.identifierThe Journal Of Endocrinology. v. 198, n. 1, p. 157-68, 2008-Jul.
dc.identifier1479-6805
dc.identifier10.1677/JOE-07-0428
dc.identifierhttp://www.ncbi.nlm.nih.gov/pubmed/18469022
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/197804
dc.identifier18469022
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1298037
dc.descriptionWe hypothesized that citrate might modulate the AMP-activated protein kinase/acetyl-CoA carboxylase (AMPK)/(ACC) pathway and participate in neuronal feeding control and glucose homeostasis. To address this issue, we injected citrate into the lateral ventricle of rats. Intracerebroventricular (ICV) injection of citrate diminished the phosphorylation of hypothalamic AMPK/ACC, increased the expression of anorexigenic neuropeptide (pro-opiomelanocortin and corticotropin-releasing hormone), elevated the level of malonyl-CoA in the hypothalamus, and reduced food intake. No change was observed in the concentration of blood insulin after the injection of citrate. With a euglycemic-hyperinsulinemic clamp, the glucose infusion rate was higher in the citrate group than in the control group (28.6+/-0.8 vs 19.3+/-0.2 mU/kg body weight/min respectively), and so was glucose uptake in skeletal muscle and the epididymal fat pad. Concordantly, insulin receptor (IR), IR substrate type 1 (IRS1), IRS2, and protein kinase B (AKT) phosphorylation in adipose tissue and skeletal muscle was improved by citrate ICV treatment. Moreover, the treatment with citrate for 7 days promoted body weight loss and decreased the adipose tissue. Our results suggest that citrate and glucose may serve as signals of energy and nutrient availability to hypothalamic cells.
dc.description198
dc.description157-68
dc.languageeng
dc.relationThe Journal Of Endocrinology
dc.relationJ. Endocrinol.
dc.rightsfechado
dc.rights
dc.sourcePubMed
dc.subjectAmp-activated Protein Kinases
dc.subjectAcetyl-coa Carboxylase
dc.subjectAnimals
dc.subjectCitric Acid
dc.subjectFeeding Behavior
dc.subjectHypothalamus
dc.subjectInjections, Intraventricular
dc.subjectInsulin
dc.subjectMale
dc.subjectPhosphorylation
dc.subjectProto-oncogene Proteins C-akt
dc.subjectRats
dc.subjectRats, Wistar
dc.subjectSignal Transduction
dc.titleIntracerebroventricular Injection Of Citrate Inhibits Hypothalamic Ampk And Modulates Feeding Behavior And Peripheral Insulin Signaling.
dc.typeArtículos de revistas


Este ítem pertenece a la siguiente institución