Impaired glucose tolerance plus hyperlipidaemia induced by diet promotes retina microaneurysms in New Zealand rabbits

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dc.contributor.author Helfenstein, Tatiana [UNIFESP]
dc.contributor.author Fonseca, Francisco A. [UNIFESP]
dc.contributor.author Ihara, Silvia S. [UNIFESP]
dc.contributor.author Bottos, Juliana M. [UNIFESP]
dc.contributor.author Moreira, Flavio T. [UNIFESP]
dc.contributor.author Pott, Henrique
dc.contributor.author Farah, Michel E. [UNIFESP]
dc.contributor.author Martins, Maria C. [UNIFESP]
dc.contributor.author Izar, Maria C. [UNIFESP]
dc.date.accessioned 2016-01-24T14:06:09Z
dc.date.available 2016-01-24T14:06:09Z
dc.date.issued 2011-02-01
dc.identifier http://dx.doi.org/10.1111/j.1365-2613.2010.00753.x
dc.identifier.citation International Journal of Experimental Pathology. Malden: Wiley-Blackwell Publishing, Inc, v. 92, n. 1, p. 40-49, 2011.
dc.identifier.issn 0959-9673
dc.identifier.uri http://repositorio.unifesp.br/handle/11600/33438
dc.description.abstract P>With the increasing prevalence of diabetes mellitus and metabolic syndrome worldwide, experimental models are required to better understand the pathophysiology and therapeutic approaches to preserve pancreatic beta cells, attenuate atherosclerosis and protect target organs. the aims of this study were to develop an experimental model of impaired glucose tolerance combined with hypercholesterolaemia induced by diet and assess metabolic alterations and target organ lesions. New Zealand male rabbits were fed high-fat/high-sucrose (10/40%) and cholesterol-enriched diet for 24 weeks, when they were sacrificed. Biochemistry, fundus photographs with fluorescein angiography and pathological analyses were performed. Cholesterol-fed and normal animals of same age were compared. Results: the animals with diet-induced impaired glucose tolerance combined with hypercholesterolaemia gained weight, increased blood glucose, total cholesterol, LDL-C and triglycerides and decreased HDL-C (P < 0.05 vs. baseline). Fructosamine levels and the homeostasis model assessment of insulin resistance (HOMA-IR) index were increased, while there was a reduction in the HOMA-beta (P < 0.05 for all vs. baseline). Histomorphologic findings of this model were aortic atherosclerosis, hepatic steatofibrosis and glomerular macrophage infiltration. Early clinical features of diabetic retinopathy with hyperfluorescent dots consistent with presence of retina microaneurysms were seen since week 12, progressing up to the end of the experiment (P < 0.0005 vs. baseline and 12 weeks). Our model reproduced several metabolic characteristics of human diabetes mellitus and promoted early signs of retinopathy. This non-expensive model is suitable for studying mechanistic pathways and allowing novel strategic approaches. en
dc.description.sponsorship Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorship Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.format.extent 40-49
dc.language.iso eng
dc.publisher Wiley-Blackwell
dc.relation.ispartof International Journal of Experimental Pathology
dc.rights Acesso restrito
dc.subject animal models en
dc.subject diet en
dc.subject impaired glucose tolerance en
dc.subject insulin resistance en
dc.subject retinopathy en
dc.title Impaired glucose tolerance plus hyperlipidaemia induced by diet promotes retina microaneurysms in New Zealand rabbits en
dc.type Artigo
dc.rights.license http://olabout.wiley.com/WileyCDA/Section/id-406071.html
dc.contributor.institution Universidade Federal de São Paulo (UNIFESP)
dc.contributor.institution Universidade Estadual de Campinas (UNICAMP)
dc.description.affiliation Universidade Federal de São Paulo, Dept Med, Div Cardiol, BR-04039030 São Paulo, Brazil
dc.description.affiliation Universidade Federal de São Paulo, Dept Ophtalmol, BR-04039030 São Paulo, Brazil
dc.description.affiliation Universidade Federal de São Paulo, Dept Pathol, BR-04039030 São Paulo, Brazil
dc.description.affiliation Pontificy Catholic Univ Campinas, São Paulo, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo, Dept Med, Div Cardiol, BR-04039030 São Paulo, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo, Dept Ophtalmol, BR-04039030 São Paulo, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo, Dept Pathol, BR-04039030 São Paulo, Brazil
dc.identifier.doi 10.1111/j.1365-2613.2010.00753.x
dc.description.source Web of Science
dc.identifier.wos WOS:000286671200005



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