HEDONICS AND DIETARY INTAKE OF FAT

心血管疾病（CVD）是死亡的主要原因， 美国人口的所有性别和种族/民族群体。水平 和餐后血脂谱是CVD的重要决定因素 风险控制餐后脂质浓度的机制是 没有充分的特点和新的证据表明，orosensory 膳食脂肪的刺激导致更高的峰值和更长的时间 与刺激相比，脂肪餐后甘油三酯（TO）升高 吃无脂食物或不吃口腔刺激物因此， 膳食脂肪的刺激可能会增加心血管疾病的风险。拟议 研究将A）确定口腔刺激的特征（例如，感官 属性，宏量营养素含量），激活导致 增加的TG浓度，B）确定口腔感觉是否 刺激对脂质产生不同程度的不同影响 C）识别个体特征（例如，基础TG 注意力集中，对感官刺激的生理反应， 选择的人格特质），可能会解释个人 血脂谱的变化，D）记录orosensory的影响 刺激与CVD风险相关的颗粒水平（例如， 极低密度脂蛋白（VLDL）和中密度脂蛋白（IDL））， 和E）确定口腔感觉刺激是否增加TG 通过增加脂质的吸收和分泌， 胃肠道，刺激TG的合成和分泌， 肝脏和/或降低TG清除率。口腔刺激的显著特征 通过监测血液成分来评估脂质负荷 在某些属性的操作之后。个人 可能与TO升高相关的特征 对口腔感觉刺激的反应性将通过 与选择的不同个体的对比结果 性状更好地了解与以下方面有关的健康风险： 饮食脂质的口腔感觉刺激将通过测量 与CVD风险相关的脂质组分。一个潜在的机制 将通过以下方式澄清对TG浓度的口腔感觉影响： 脂质负荷的控制（胃内与静脉内）和测量 特定的载脂蛋白（apoB-48，apoB-100）和标记物， 棕榈酸盐

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.