HEDONICS AND DIETARY INTAKE OF FAT

心血管疾病(CVD)是#年死亡的主要原因。 美国人口中的所有性别和种族/民族。关卡 和餐后血脂水平是心血管疾病的重要决定因素 风险。控制餐后血脂浓度的机制是 没有完全表征和新的证据表明，味觉 饮食脂肪的刺激会导致更高的峰值和更长的时间 脂肪餐后甘油三酯(TO)的升高比刺激 有脱脂食物或无口腔刺激。因此，味觉 饮食脂肪的刺激可能会增加心血管疾病的风险。建议数 研究将A)确定口腔刺激的特征(例如，感觉 属性、常量营养素含量)，这些激活过程导致 增加甘油三酯浓度，B)确定口感 刺激对不同程度的血脂有不同的影响 C)识别个体特征(例如，基础Tg 注意力，对感官刺激的生理反应， 选定的个性特征)，这可能解释了个人 脂类分布的可变性，D)记录味觉的影响 对与心血管疾病风险相关的颗粒物水平的刺激(例如， 极低密度脂蛋白(VLDL)和中等密度脂蛋白(IDL))， 和E)确定味觉刺激是否增加TG 通过增加脂肪的吸收和分泌来浓缩 胃肠轨迹，刺激甘油三酯的合成和分泌 肝脏和/或减少甘油三酯清除。口述刺激的显著特征 并将通过监测血液成分来评估脂质负荷 在对某些属性进行操作之后。个体 可能与增强到 对味觉刺激的反应将通过以下方式确定 对比所获得的结果与所选择的个体的不同 特征。提高对与以下疾病相关的健康风险的认识 通过测量食物中的脂肪来获得嗅觉刺激。 与心血管疾病风险相关的脂组分。一种潜在的机制 感官对甘油三酯浓度的影响将通过 脂类负荷的控制(胃和静脉)和测量 特定的载脂蛋白(apoB-48、apoB-100)和标记视黄醇 棕榈酸。

Cardiovascular diseases (CVD) are the leading causes of mortality in all gender and racial/ethnic groups of the U.S. population. The level and profile of postprandial lipids are important determinants of CVD risk. The mechanisms controlling postprandial lipid concentrations are not fully characterized and new evidence indicates that orosensory stimulation with dietary fat leads to a higher peak and more prolonged elevation of triglycerides (TO) after a lipid meal than stimulation with a non-fat food or no oral stimulation. Consequently, orosensory stimulation by dietary fat may contribute to CVD risk. The proposed studies will A) determine features of the oral stimulus (e.g., sensory properties, macronutrient content) that activate processes leading to augmented TG concentrations, B) ascertain whether orosensory stimulation exerts a differential effect on lipids varying in degree of saturation, C) identify individual characteristics (e.g., basal TG concentration, physiological responsiveness to sensory stimulation, selected personality traits) that may account for individual variability in lipid profiles, D) document the effects of orosensory stimulation on levels of particles associated with CVD risk (e.g., very-low-density- (VLDL) and intermediate-density-lipoproteins (IDL)), and E) establish whether orosensory stimulation augments the TG concentration by increasing lipid absorption and secretiOn from the gastrointestinal track, stimulating TG synthesis and secretion from the liver and/or reducing TG clearance. Salient features of oral stimuli and lipid loads will be assessed by monitoring blood constituents following manipulations of certain attributes. Individual characteristics that may be associated with heightened TO responsiveness to orosensory stimulation will be identified by contrasting findings obtained with individuals varying on selected traits. An improved understanding of the health risks related to orosensory stimulation by dietary lipids will be obtained by measuring lipid fractions associated with CVD risk. The mechanism underlying an orosensory influence on TG concentration will be clarified through control of lipid loading (gastric versus intravenous) and measurement of specific apoproteins (apoB-48, apoB-100) and a marker, retinyl palmitate.