Causes of cafeteria-feeding obesity
Causes of cafeteria-feeding obesity
批准号:
10355497
负责人:
MICHAEL G TORDOFF
金额:
$32.99万
依托单位国家:
美国
项目类别:
财政年份:
2020
资助国家:
美国
项目状态:
已结题
起止时间:
2020-04-10 至 2023-02-28
关键词:
Animal ExperimentsAnimal ModelAttentionBody WeightCanola OilCarbohydratesClinicalConsumptionCorn starch preparationDietEatingExposure toFat-Restricted DietFatty acid glycerol estersFoodFood SelectionsFosteringGeneticGlycemic IndexHealthHigh Fat DietHumanInvestigationKnowledgeMacronutrients NutritionMaintenanceMetabolicModelingMonitorMusObese MiceObesityPhysiologicalResearchRodentRodent ModelSourceStarchStimulusStudy modelsSucroseSupermarketTimeUnited StatesVegetablesWeightWeight GainWorkbasedietaryeconomic impactenergy densityexperienceexperimental studyfeedingfollow-uphuman modelinsightnovelpalm oilrelating to nervous systemsugar
中文摘要
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英文摘要
PROJECT SUMMARY/ABSTRACT
Rodents offered a cafeteria choice of two or more “supermarket” foods gain substantially more weight than if
fed only one such food. This “cafeteria-feeding” model captures aspects of human obesity that are missing
from other rodent models, but the use of prepared human foods adds complexity that precludes meaningful
analysis and interpretation. We have developed a simpler and more rigorous model to investigate the causes
of the heightened obesity imparted by cafeteria feeding. Mice offered a choice between a high-carbohydrate,
low-fat diet and an equicaloric low-carbohydrate, high-fat diet gain substantially more weight than do mice fed
either diet alone. To characterize and establish this new model, we will determine the range of proportions of
carbohydrate and fat that support the extra weight gain (Aim 1), investigate whether various sources of
carbohydrate and fat are equally effective (Aim 2), determine whether mice actively select carbohydrate and fat
diets that maximize their obesity (Aim 3), and investigate the temporal aspects of the carbohydrate-fat
interaction by switching mice between high-carbohydrate and high-fat diets at various intervals, including
between successive meals and within meals (Aim 4). These and related follow-up experiments will give insight
into the causes of cafeteria-feeding obesity, and set the stage for the identification of the underlying
physiological mechanisms. The mouse cafeteria-feeding paradigm has obvious direct parallels to the human
experience. As such, this project will yield an animal model that can be exploited to investigate the
physiological, neural and genetic mechanisms responsible for the “extra” obesity caused by cafeteria feeding.
It will thus establish a more faithful model of human obesity than those currently available.
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