| Autor: |
Melo BF; CEDOC, NOVA Medical School, Faculdade de Ciências Médicas, 1150-082 Lisboa, Portugal. Bernardete.melo@nms.unl.pt., Sacramento JF; CEDOC, NOVA Medical School, Faculdade de Ciências Médicas, 1150-082 Lisboa, Portugal. joana.sacramento@nms.unl.pt., Ribeiro MJ; CEDOC, NOVA Medical School, Faculdade de Ciências Médicas, 1150-082 Lisboa, Portugal. mj.rfribeiro@gmail.com., Prego CS; CEDOC, NOVA Medical School, Faculdade de Ciências Médicas, 1150-082 Lisboa, Portugal. claudia.prego@nms.unl.pt., Correia MC; CEDOC, NOVA Medical School, Faculdade de Ciências Médicas, 1150-082 Lisboa, Portugal. mc.correia@campus.fct.unl.pt., Coelho JC; CEDOC, NOVA Medical School, Faculdade de Ciências Médicas, 1150-082 Lisboa, Portugal. joana.indias@gmail.com., Cunha-Guimaraes JP; CEDOC, NOVA Medical School, Faculdade de Ciências Médicas, 1150-082 Lisboa, Portugal. jp.guimaraes@campus.fct.unl.pt., Rodrigues T; Instituto de Investigação Clínica e Biomédica de Coimbra (iCBR), Faculdade de Medicina de Coimbra, 3000-548 Coimbra, Portugal. tiagodarodrigues@gmail.com., Martins IB; CEDOC, NOVA Medical School, Faculdade de Ciências Médicas, 1150-082 Lisboa, Portugal. iib.martins@campus.fct.unl.pt., Guarino MP; CEDOC, NOVA Medical School, Faculdade de Ciências Médicas, 1150-082 Lisboa, Portugal. maria.guarino@ioleiria.pt.; Escola Superior de Saúde de Leiria- Instituto Politécnico de Leiria, 2410-197 Leiria, Portugal. maria.guarino@ioleiria.pt., Seiça RM; Instituto de Investigação Clínica e Biomédica de Coimbra (iCBR), Faculdade de Medicina de Coimbra, 3000-548 Coimbra, Portugal. rmfseica@gmail.com., Matafome P; Instituto de Investigação Clínica e Biomédica de Coimbra (iCBR), Faculdade de Medicina de Coimbra, 3000-548 Coimbra, Portugal. paulomatafome@gmail.com.; Instituto Politécnico de Coimbra, Coimbra Health School (ESTeSC), Department of Complementary Sciences, 3046-854 Coimbra, Portugal. paulomatafome@gmail.com., Conde SV; CEDOC, NOVA Medical School, Faculdade de Ciências Médicas, 1150-082 Lisboa, Portugal. silvia.conde@nms.unl.pt. |
| Abstrakt: |
Animal experimentation has a long history in the study of metabolic syndrome-related disorders. However, no consensus exists on the best models to study these syndromes. Knowing that different diets can precipitate different metabolic disease phenotypes, herein we characterized several hypercaloric rat models of obesity and type 2 diabetes, comparing each with a genetic model, with the aim of identifying the most appropriate model of metabolic disease. The effect of hypercaloric diets (high fat (HF), high sucrose (HSu), high fat plus high sucrose (HFHSu) and high fat plus streptozotocin (HF+STZ) during different exposure times (HF 3 weeks, HF 19 weeks, HSu 4 weeks, HSu 16 weeks, HFHSu 25 weeks, HF3 weeks + STZ) were compared with the Zucker fatty rat. Each model was evaluated for weight gain, fat mass, fasting plasma glucose, insulin and C-peptide, insulin sensitivity, glucose tolerance, lipid profile and liver lipid deposition, blood pressure, and autonomic nervous system function. All animal models presented with insulin resistance and dyslipidemia except the HF+STZ and HSu 4 weeks, which argues against the use of these models as metabolic syndrome models. Of the remaining animal models, a higher weight gain was exhibited by the Zucker fatty rat and wild type rats submitted to a HF diet for 19 weeks. We conclude that the latter model presents a phenotype most consistent with that observed in humans with metabolic disease, exhibiting the majority of the phenotypic features and comorbidities associated with type 2 diabetes in humans. |
