title: Mouse strain-dependent variation in obesity and glucose homeostasis in response to high-fat feeding.
abstract: OBJECTIVE
  Metabolic disorders are commonly investigated using knockout and transgenic mouse models. A variety of mouse strains have been used for this purpose. However, mouse strains can differ in their inherent propensities to develop metabolic disease, which may affect the experimental outcomes of metabolic studies. We have investigated strain-dependent differences in the susceptibility to diet-induced obesity and insulin resistance in five commonly used inbred mouse strains (C57BL/6J, 129X1/SvJ, BALB/c, DBA/2 and FVB/N).
  
  
  METHODS
  Mice were fed either a low-fat or a high-fat diet (HFD) for 8 weeks. Whole-body energy expenditure and body composition were then determined. Tissues were used to measure markers of mitochondrial metabolism, inflammation, oxidative stress and lipid accumulation.
  
  
  RESULTS
  BL6, 129X1, DBA/2 and FVB/N mice were all susceptible to varying degrees to HFD-induced obesity, glucose intolerance and insulin resistance, but BALB/c mice exhibited some protection from these detrimental effects. This protection could not be explained by differences in mitochondrial metabolism or oxidative stress in liver or muscle, or inflammation in adipose tissue. Interestingly, in contrast with the other strains, BALB/c mice did not accumulate excess lipid (triacylglycerols and diacylglycerols) in the liver; this is potentially related to lower fatty acid uptake rather than differences in lipogenesis or lipid oxidation.
  
  
  CONCLUSIONS
  Collectively, our findings indicate that most mouse strains develop metabolic defects on an HFD. However, there are inherent differences between strains, and thus the genetic background needs to be considered carefully in metabolic studies.
authors: Diabetes and Obesity Research Program, Garvan Institute of Medical Research, 384 Victoria St., Darlinghurst, Sydney, NSW 2010, Australia.
authors: M K
authors: MK
authors: Montgomery
authors: N L
authors: NL
authors: Hallahan
authors: S H
authors: SH
authors: Brown
authors: M
authors: M
authors: Liu
authors: T W
authors: TW
authors: Mitchell
authors: G J
authors: GJ
authors: Cooney
authors: N
authors: N
authors: Turner
mesh_terms: D002001:Adipose Tissue, Brown / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D052436:Adipose Tissue, White / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D050154:Adiposity; D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D059305:Diet, High-Fat / Q000009:adverse effects*; D004198:Disease Susceptibility; D018149:Glucose Intolerance / Q000209:etiology* / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D007333:Insulin Resistance; D050356:Lipid Metabolism; D008099:Liver / Q000201:enzymology / Q000378:metabolism*; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D008928:Mitochondria / Q000201:enzymology / Q000378:metabolism; D018482:Muscle, Skeletal / Q000201:enzymology / Q000378:metabolism; D009765:Obesity / Q000209:etiology* / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D018384:Oxidative Stress; D011897:Random Allocation; D013045:Species Specificity
chemical_list: D015415:Biomarkers