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Is the FVB/N mouse strain truly resistant to diet‐induced obesity?

C57Bl/6J mice are the gold standard animal model of diet‐induced obesity. These animals become obese with higher adiposity, blood fasting glucose, triglycerides, and total cholesterol when fed a high‐fat diet (HFD). Conversely, the FVB/N mouse line is thought to be resistant to diet‐induced obesity,...

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Detalles Bibliográficos
Autores principales: Nascimento‐Sales, Michelle, Fredo‐da‐Costa, Izabelle, Borges Mendes, Adriane C. B., Melo, Suzane, Ravache, Thais T., Gomez, Thiago G. B., Gaisler‐Silva, Fernanda, Ribeiro, Miriam O., Santos, Arnaldo R., Carneiro‐Ramos, Marcela S., Christoffolete, Marcelo A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5430125/
https://www.ncbi.nlm.nih.gov/pubmed/28483861
http://dx.doi.org/10.14814/phy2.13271
Descripción
Sumario:C57Bl/6J mice are the gold standard animal model of diet‐induced obesity. These animals become obese with higher adiposity, blood fasting glucose, triglycerides, and total cholesterol when fed a high‐fat diet (HFD). Conversely, the FVB/N mouse line is thought to be resistant to diet‐induced obesity, with low or no weight gain and adiposity in response to a HFD. In this study, we investigated whether FVB/N mice are resistant or susceptible to metabolic disorder that is promoted by a HFD. Biometric parameters and blood chemistry were analyzed in C57Bl/6J and FVB/N mice that were fed a chow diet or HFD. Glucose and insulin sensitivity were assessed by performing the glucose tolerance test and measuring serum insulin/glucose and homeostasis model assessment‐insulin resistance. Metabolism‐related gene expression was investigated by real‐time reverse transcription polymerase chain reaction. Adipocyte morphology and liver steatosis were evaluated using standard histology. FVB/N mice had higher adiposity than C57Bl/6J mice that were fed a chow diet and were glucose intolerant. FVB/N mice that were fed a HFD presented higher insulin resistance and greater liver steatosis. Epididymal white adipose tissue exhibited severe inflammation in FVB/N mice that were fed a HFD. The FVB/N mouse strain is suitable for studies of diet‐induced obesity, and the apparent lack of a HFD‐induced response may reveal several strain‐specific events that are triggered by a HFD. Further studies of the FVB/N background may shed light on the complex multifactorial symptoms of obesity and metabolic syndrome.