Causes of cafeteria-feeding obesity

食堂肥胖的原因

• 批准号: 10355497
• 负责人: MICHAEL G TORDOFF
• 金额: $ 32.99万
• 依托单位: MONELL CHEMICAL SENSES CENTER
• 依托单位国家: 美国
• 财政年份: 2020
• 资助国家: 美国
• 起止时间: 2020-04-10 至 2023-02-28
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/10355497
• 关键词: Animal Experiments; Animal Model; Attention; Body Weight; Canola Oil; Carbohydrates; Clinical; Consumption; Corn starch preparation; Diet; Eating; Exposure to; Fat-Restricted Diet; Fatty acid glycerol esters; Food; Food Selections; Fostering; Genetic; Glycemic Index; Health; High Fat Diet; Human; Investigation; Knowledge; Macronutrients Nutrition; Maintenance; Metabolic; Modeling; Monitor; Mus; Obese Mice; Obesity; Physiological; Research; Rodent; Rodent Model; Source; Starch; Stimulus; Study models; Sucrose; Supermarket; Time; United States; Vegetables; Weight; Weight Gain; Work; base; dietary; economic impact; energy density; experience; experimental study; feeding; follow-up; human model; insight; novel; palm oil; relating to nervous system; sugar

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.

项目概要/摘要 给啮齿类动物提供两种或两种以上“超市”食物的选择，其体重比如果提供更多的体重 只喂一种这样的食物，这种“自助餐厅喂食”模型捕捉到了人类肥胖所缺失的方面。 与其他啮齿动物模型不同，但使用准备好的人类食物增加了复杂性，从而排除了有意义的 我们开发了一个更简单、更严格的模型来调查原因。 食堂喂养造成的肥胖症小鼠可以在高碳水化合物、 低脂饮食和等热量的低碳水化合物、高脂肪饮食比喂食的小鼠体重增加得多 为了描述和建立这个新模型，我们将确定饮食的比例范围。 支持额外体重增加的碳水化合物和脂肪（目标 1），是否调查各种来源 碳水化合物和脂肪同样有效（目标2），确定小鼠是否主动选择碳水化合物和脂肪 最大限度地提高肥胖率的饮食（目标 3），并研究碳水化合物-脂肪的时间方面 通过以不同的时间间隔在高碳水化合物和高脂肪饮食之间切换小鼠来相互作用，包括 连续进餐之间和进餐期间（目标 4）。这些和相关的后续实验将提供见解。 探究食堂肥胖的原因，并为识别根本原因奠定基础 小鼠食堂喂养模式与人类有明显的直接相似之处。 因此，该项目将产生一个可用于研究的动物模型。 食堂用餐导致“额外”肥胖的生理、神经和遗传机制。 因此，它将建立一个比现有模型更忠实的人类肥胖模型。