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Dietary obesity in nine inbred mouse strains
486
Citations
13
References
1992
Year
NutritionGeneticsWk ConsumptionExperimental NutritionObesityMetabolic SyndromeBody CompositionMarginal EffectMolecular NutritionPublic HealthAnimal PhysiologyLipid NutritionAnimal NutritionDietary ObesityCm DietPhysiologyFeed IntakeMetabolismMedicine
Identifying inbred mouse strains that are sensitive versus resistant to dietary obesity provides a useful tool for exploring the metabolic and genetic basis of this trait. The study evaluated the effect of a 7‑week, 32.6 % fat condensed‑milk diet on body composition and energy intake in nine inbred mouse strains. Control animals received a high‑carbohydrate chow diet (11.6 % fat) while the experimental group received the condensed‑milk diet, allowing comparison over the 7‑week period. Compared to chow controls, the condensed‑milk diet increased carcass lipid in six strains but not in three, and the obesity was not driven by hyperphagia, as only one of the six leaner strains (AKR/J) consumed more energy.
The effect of 7 wk consumption of a diet containing 32.6% of kilocalories as fat [condensed milk (CM) diet] on body composition and energy intake was evaluated in nine strains of inbred mice (AKR/J, C57L/J, A/J, C3H/HeJ, DBA/2J, C57BL/6J, SJL/J, I/STN, and SWR/J). Control animals were fed a high-carbohydrate diet containing 11.6% of energy as fat (Purina Rodent Chow diet). Relative to Chow diet controls, the CM diet significantly increased carcass lipid content in six strains (AKR/J, C57L/J, A/J, C3H/HeJ, DBA/2J, and C57BL/6J), but had no or a marginal effect on adiposity in three strains of mice (SJL/J, I/STN, and SWR/J). The obesity produced by the CM diet in six strains was not due to hyperphagia. Only one of six (AKR/J) of the strains that increased adiposity on the CM diet consumed more energy than controls during the 7 wk of the experiment. The identification of inbred mouse strains that are sensitive to dietary obesity, vs. others that are resistant, provides a useful tool to pursue the metabolic and genetic basis of this trait in the mouse.
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