Fatty acid sources of fructose and HFCS-induced postprandial hypertriglyceridemia

果糖的脂肪酸来源和 HFCS 诱发的餐后高甘油三酯血症

基本信息

批准号：
8680329
负责人：
PETER J HAVEL
金额：
$ 35.56万
依托单位：
UNIVERSITY OF CALIFORNIA AT DAVIS
依托单位国家：
美国
项目类别：
财政年份：
2011
资助国家：
美国
起止时间：
2011-09-01 至 2017-06-30
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/8680329
关键词：
Adipose tissue Adult Ancillary Study Apolipoproteins B Aspartame Blood specimen Carbohydrates Cardiovascular Diseases Characteristics Clinical Research Complex Consumption Data Development Diabetes Mellitus Diet Dietary Intervention Dose Epidemiology Fasting Fatty Acids Fructose Funding Glucose Hour Hypertriglyceridemia Incidence Inpatients Insulin Resistance Intake Intervention Intravenous infusion procedures Investigation LDL Cholesterol Lipoproteins Lead Link Lipids Lipolysis Lipoproteins Low-Density Lipoproteins Measurement Metabolic Metabolic Diseases Metabolic syndrome Methodology National Heart, Lung, and Blood Institute Non-Insulin-Dependent Diabetes Mellitus Nonesterified Fatty Acids Obesity Oral Overweight Parents Participant Plasma Procedures Production Protocols documentation Regimen Risk Factors Source Testing Tracer Triglycerides United States National Institutes of Health Weight abstracting cardiovascular risk factor energy balance feeding insight lipid biosynthesis novel stable isotope sugar sweetened beverage young man young woman

项目摘要

DESCRIPTION (provided by applicant): The parent study for this proposed ancillary study is an NIH/NHLBI-funded investigation comparing the effects of consuming sweetened beverages for 2 weeks in young (18-40 years), normal weight and overweight/obese adults (5R01HL091333-02: Effects of 2wk fructose & HFCS consumption on lipid dysregulation & insulin resistance). Baseline experimental procedures (including 24-h serial blood sampling) are conducted while subjects reside as inpatients at the CTSC-funded Clinical Research Center (CCRC) for 3.5 days and consume an energy-balanced, high complex carbohydrate diet. Subjects then consume sweetened beverages providing 25% of energy requirements as fructose, glucose, or high fructose corn syrup (HFCS); or 0, 10, or 17.5% of energy as fructose or HFCS along with their usual ad libitum diet. At the end of the 2-week intervention, subjects return to the CCRC and the same experimental procedures are performed while subjects consume an energy-balanced diet, which includes the assigned sweetened beverages. The early results from this investigation indicate that consumption of HFCS-sweetened beverages at 25% of energy results in significant increases of late-night postprandial triglyceride (TG) concentrations, and of fasting LDL cholesterol and apolipoprotein-B (ApoB) concentrations that are comparable in magnitude to those observed after consumption of beverages sweetened with 100% fructose. Consumption of glucose-sweetened beverages does not alter these parameters. There is considerable evidence to support the hypothesis that postprandial hypertriglyceridemia is a key metabolic disturbance that gives rise to the lipid dysregulation characteristic of metabolic syndrome and type 2 diabetes. The purpose of this proposal is to investigate the mechanisms that contribute to the postprandial hypertriglyceridemia induced by fructose and HFCS consumption by quantifying the absolute and proportional contributions of fatty acids derived from de novo lipogenesis (DNL), diet, and free fatty acids (FFA) from adipose TG lipolysis to fasting and postprandial levels of triglyceride-rich lipoproteins (TRL). Stable isotopes will be administered (via oral consumption and 26-h intravenous infusions) to subsets of subjects during the 24-h serial blood sampling protocols that are conducted in all study participants during consumption of energy-balanced, high complex carbohydrate meals at baseline, and meals consumed with beverages sweetened with HFCS, fructose, glucose or aspartame at the end of intervention. The specific objective of these studies is to test the hypothesis that 2 weeks of fructose or HFCS consumption will increase the absolute and proportional contributions of fatty acids derived from DNL to late-night increases of TRL, and that the increases of DNL-fatty acid will be a critical determinant of the increases of fasting LDL and ApoB concentrations. A second objective is to determine the doses of HFCS that increase the absolute and proportional contributions of DNL-fatty acids to postprandial TRL.

描述（由申请人提供）：这项拟议的辅助研究的父母研究是NIH/NHLBI资助的研究，比较了年轻（18-40岁）（18-40岁），正常体重和超重/肥胖的成年人2周的消耗甜味饮料的影响（5R01HL01HL01HL091333-02：2WK Fimption＆HFCS intrection＆Hfcs in lip）的影响。在CTSC资助的临床研究中心（CCRC）中，进行了3.5天，而受试者作为住院病人居住，进行了基线实验程序（包括24小时连续抽样），并消耗能量平衡，高复杂的碳水化合物饮食。然后，受试者食用甜味饮料，提供25％的能量需求，例如果糖，葡萄糖或高果糖玉米糖浆（HFCS）；或0、10或17.5％的能量作为果糖或HFC，以及通常的特征饮食。在2周的干预结束时，受试者返回CCRC，并且在受试者消耗能量平衡饮食的同时，进行了相同的实验程序，其中包括指定的甜味饮料。这项研究的早期结果表明，以能量的25％的25％的饮料消费会导致深夜餐后甘油三酸酯（TG）浓度显着增加，而禁食的LDL胆固醇和载脂蛋白-B（APOB）浓度与量相比，与量相比，与量相比，与量相比，量较高后，与饮食量相当。消费葡萄糖甜饮料不会改变这些参数。有大量证据支持以下假设：餐后高糖性血症是一种关键的代谢障碍，引起了代谢综合征和2型糖尿病的脂质失调特征。 The purpose of this proposal is to investigate the mechanisms that contribute to the postprandial hypertriglyceridemia induced by fructose and HFCS consumption by quantifying the absolute and proportional contributions of fatty acids derived from de novo lipogenesis (DNL), diet, and free fatty acids (FFA) from adipose TG lipolysis to fasting and postprandial levels of triglyceride-rich脂蛋白（TRL）。在24小时的连续血液采样方案中，将对所有研究参与者进行稳定的同位素（通过口服消耗和26小时的静脉输注）对受试者的子集进行管理，这些方案在基线时消费，高能量的碳水化合物粉的消费量，并与HFCS，Glucose，gluceSe gluce of ass gluce of ass gluce a ans vers contections contine contements conseptress。这些研究的具体目的是检验以下假设：果糖或HFCS消耗的2周将增加脂肪酸对TRL深夜增加的脂肪酸的绝对和比例贡献，并且DNL-fatty Acid的增加将是禁食LDL和APOB浓度增加的关键决定性。第二个目标是确定HFC的剂量，以增加DNL-Fatty酸对餐后TRL的绝对和比例贡献。