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High-fat feeding rapidly induces obesity and lipid derangements in C57BL/6N mice |
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| Authors: | Christine Podrini Emma L. Cambridge Christopher J. Lelliott Damian M. Carragher Jeanne Estabel Anna-Karin Gerdin Natasha A. Karp Cheryl L. Scudamore Ramiro Ramirez-Solis Jacqueline K. White |
| Affiliation: | 1. Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridgeshire, CB10 1SA, UK 2. Epigenetics of Fatty Liver Disease Research Group, Institute of Hepatology, Foundation for Liver Research, 69-75 Chenies Mews, London, WC1E 6HX, UK 3. Division of Immunoregulation, MRC National Institute for Medical Research (NIMR), The Ridgeway, Mill Hill, London, NW7 1AA, UK 4. Department of Pathology and Infectious Diseases, Royal Veterinary College, Hawkshead Lane, North Mymms, Hatfield, Hertfordshire, AL9 7TA, UK 5. MRC Harwell, Harwell Science and Innovation Campus, Harwell, Oxfordshire, OX11 0RD, UK |
| Abstract: | C57BL/6N (B6N) is becoming the standard background for genetic manipulation of the mouse genome. The B6N, whose genome is very closely related to the reference C57BL/6J genome, is versatile in a wide range of phenotyping and experimental settings and large repositories of B6N ES cells have been developed. Here, we present a series of studies showing the baseline characteristics of B6N fed a high-fat diet (HFD) for up to 12 weeks. We show that HFD-fed B6N mice show increased weight gain, fat mass, and hypercholesterolemia compared to control diet-fed mice. In addition, HFD-fed B6N mice display a rapid onset of lipid accumulation in the liver with both macro- and microvacuolation, which became more severe with increasing duration of HFD. Our results suggest that the B6N mouse strain is a versatile background for studying diet-induced metabolic syndrome and may also represent a model for early nonalcoholic fatty liver disease. |
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