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Mice long-term high-fat diet feeding recapitulates human cardiovascular alterations: an animal model to study the early phases of diabetic cardiomyopathy

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dc.contributor.author Calligaris, Sebastian
dc.contributor.author Lecanda, Manuel
dc.contributor.author Solis, Felipe
dc.contributor.author Ezquer, Marcelo
dc.contributor.author Gutierrez, Jaime
dc.contributor.author Brandan, Enrique
dc.contributor.author Leiva, Andrea
dc.contributor.author Sobrevia, Luis
dc.contributor.author Conget, Paulette
dc.date.accessioned 2017-04-07T16:00:12Z
dc.date.available 2017-04-07T16:00:12Z
dc.date.issued 2013
dc.identifier.citation PLoS One. 2013; 8(4): e60931
dc.identifier.uri http://hdl.handle.net/11447/1115
dc.identifier.uri http://dx.doi.org/10.1371/journal.pone.0060931
dc.description Centro de Medicina Regenerativa
dc.description.abstract BACKGROUND/AIM: Hypercaloric diet ingestion and sedentary lifestyle result in obesity. Metabolic syndrome is a cluster of clinical features secondary to obesity, considered as a pre-diabetic condition and recognized as an independent risk factor for cardiovascular diseases. To better understand the relationship between obesity, metabolic syndrome and cardiovascular disease as well as for the development of novel therapeutic strategies, animal models that reproduce the etiology, course and outcomes of these pathologies are required. The aim of this work was to characterize the long-term effects of high-fat diet-induced obesity on the mice cardiovascular system, in order to make available a new animal model for diabetic cardiomyopathy. METHODS/RESULTS: Male C57BL/6 mice were fed with a standardized high-fat diet (obese) or regular diet (normal) for 16 months. Metabolic syndrome was evaluated testing plasma glucose, triglycerides, cholesterol, insulin, and glucose tolerance. Arterial pressure was measured using a sphygmomanometer (non invasive method) and by hemodynamic parameters (invasive method). Cardiac anatomy was described based on echocardiography and histological studies. Cardiac function was assessed by cardiac catheterization under a stress test. Cardiac remodelling and metabolic biomarkers were assessed by RT-qPCR and immunoblotting. As of month eight, the obese mice were overweight, hyperglycaemic, insulin resistant, hyperinsulinemic and hypercholesterolemic. At month 16, they also presented normal arterial pressure but altered vascular reactivity (vasoconstriction), and cardiac contractility reserve reduction, heart mass increase, cardiomyocyte hypertrophy, cardiac fibrosis, and heart metabolic compensations. By contrast, the normal mice remained healthy throughout the study. CONCLUSIONS: Mice fed with a high-fat diet for prolonged time recapitulates the etiology, course and outcomes of the early phases of human diabetic cardiomyopathy.
dc.format.extent 10
dc.language.iso en_US
dc.publisher PLoS
dc.subject Diabetic Cardiomyopathies/physiopathology
dc.subject Disease Models, Animal
dc.subject Metabolic Syndrome X/physiopathology
dc.subject Obesity/physiopathology
dc.subject Diet, High-Fat
dc.title Mice long-term high-fat diet feeding recapitulates human cardiovascular alterations: an animal model to study the early phases of diabetic cardiomyopathy
dc.type Artículo


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