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.

项目摘要/摘要 啮齿动物提供了两种或多种“超市”食品的自助餐厅，比 只喂这样的食物。这种“自助餐厅喂养”模型捕捉了缺少人类肥胖的各个方面 来自其他啮齿动物模型，但使用准备的人类食品的使用增加了不可能有意义的复杂性 分析和解释。我们已经开发了一个更简单，更严格的模型来研究原因 自助餐厅喂养赋予的肥胖增强。小鼠提供了高碳水化合物之间的选择， 低脂饮食和相等的低碳水化合物，高脂饮食的体重比喂养的小鼠大得多 要么一个饮食。为了表征和建立这个新模型，我们将确定比例的范围 支持额外的体重增加的碳水合物和脂肪（AIM 1），研究各种来源是否来源 碳水合物和脂肪同样有效（AIM 2），确定小鼠是否积极选择碳水和脂肪 最大化其肥胖症的饮食（AIM 3），并研究碳水化合物脂肪的临时方面 通过以不同的间隔在高碳水化合物和高脂饮食之间切换小鼠的相互作用，包括 在成功的饭菜和饭菜之间（目标4）。这些和相关的后续实验将提供洞察力 进入自助餐厅喂肥胖的原因，并为识别基础奠定了基础 生理机制。小鼠自助餐厅喂养范式与人类具有明显的直接相似之处 经验。因此，该项目将产生一个可以探索的动物模型以调查 造成自助餐厅喂养引起的“额外”肥胖的生理，神经和遗传机制。 因此，它将建立比当前可用的肥胖模型更忠实的模型。