Primary Hypercholesterolaemia Impairs Glucose Homeostasis And Insulin Secretion In Low-density Lipoprotein Receptor Knockout Mice Independently Of High-fat Diet And Obesity.

dc.creatorBonfleur, Maria Lúcia
dc.creatorVanzela, Emerielle Cristine
dc.creatorRibeiro, Rosane Aparecida
dc.creatorde Gabriel Dorighello, Gabriel
dc.creatorde França Carvalho, Carolina Prado
dc.creatorCollares-Buzato, Carla Beatriz
dc.creatorCarneiro, Everardo Magalhães
dc.creatorBoschero, Antonio Carlos
dc.creatorde Oliveira, Helena Coutinho Franco
dc.date2010-Feb
dc.date2015-11-27T13:18:33Z
dc.date2015-11-27T13:18:33Z
dc.date.accessioned2018-03-29T01:12:11Z
dc.date.available2018-03-29T01:12:11Z
dc.identifierBiochimica Et Biophysica Acta. v. 1801, n. 2, p. 183-90, 2010-Feb.
dc.identifier0006-3002
dc.identifier10.1016/j.bbalip.2009.10.012
dc.identifierhttp://www.ncbi.nlm.nih.gov/pubmed/19913637
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/199188
dc.identifier19913637
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1299421
dc.descriptionWe investigated whether primary hypercholesterolaemia per se affects glucose homeostasis and insulin secretion in low-density lipoprotein receptor knockout mice (LDLR(-/-)). Glucose plasma levels were increased and insulin decreased in LDLR(-/-) compared to the wild-type mice. LDLR(-/-) mice presented impaired glucose tolerance, but normal whole body insulin sensitivity. The dose-response curve of glucose-stimulated insulin secretion was shifted to the right in LDLR(-/-) islets. Significant reductions in insulin secretion in response to l-leucine or 2-ketoisocaproic acid were also observed in LDLR(-/-). Islet morphometric parameters, total insulin and DNA content were similar in both groups. Glucose uptake and oxidation were reduced in LDLR(-/-) islets. Removal of cholesterol from LDLR(-/-) islets corrected glucose-stimulated insulin secretion. These results indicate that enhanced membrane cholesterol content due to hypercholesterolaemia leads to a lower insulin secretion and glucose intolerance without affecting body insulin sensitivity. This represents an additional risk factor for diabetes and atherosclerosis in primary hypercholesterolaemia.
dc.description1801
dc.description183-90
dc.languageeng
dc.relationBiochimica Et Biophysica Acta
dc.relationBiochim. Biophys. Acta
dc.rightsfechado
dc.rights2009 Elsevier B.V. All rights reserved.
dc.sourcePubMed
dc.subjectAnimals
dc.subjectCholesterol
dc.subjectDietary Fats
dc.subjectFemale
dc.subjectGlucose
dc.subjectGlucose Tolerance Test
dc.subjectHomeostasis
dc.subjectHypercholesterolemia
dc.subjectInsulin
dc.subjectIslets Of Langerhans
dc.subjectLeucine
dc.subjectLipids
dc.subjectMale
dc.subjectMice
dc.subjectMice, Knockout
dc.subjectObesity
dc.subjectOxidation-reduction
dc.subjectReceptors, Ldl
dc.subjectBeta-cyclodextrins
dc.titlePrimary Hypercholesterolaemia Impairs Glucose Homeostasis And Insulin Secretion In Low-density Lipoprotein Receptor Knockout Mice Independently Of High-fat Diet And Obesity.
dc.typeArtículos de revistas


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