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

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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, Jr., Arnaldo R. ; Carneiro-Ramos, Marcela S. ; Christoffolete, Marcelo A.

• Tipo de documento: Artigo Científico
• Fonte: PHYSIOLOGICAL REPORTS; v. 5, n. 9 MAY 2017.
• Citações Web of Science: 2

Resumo

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. (AU)

• Processo FAPESP: 15/02052-3 - Estudo do papel do receptor TrkB no desenvolvimento de doença hepática gordurosa não alcoólica (DHGNA) em camundongos
• Beneficiário: Marcelo Augusto Christoffolete
• Linha de fomento: Auxílio à Pesquisa - Regular
• Processo FAPESP: 08/10700-1 - Homeostase energética em diferentes linhagens de camundongos: influência da alimentação, miméticos da atividade física e genética
• Beneficiário: Marcelo Augusto Christoffolete
• Linha de fomento: Auxílio à Pesquisa - Apoio a Jovens Pesquisadores