University of Adelaide Discipline of Medicine, Adelaide, Australia; South Australian Health and Medical Research Institute, Adelaide, Australia; NHMRC Centre of Research Excellence in Translating Nutritional Science to Good Health, University of Adelaide, Adelaide, Australia.
University of Adelaide Discipline of Medicine, Adelaide, Australia; South Australian Health and Medical Research Institute, Adelaide, Australia.
Clin Nutr. 2017 Apr;36(2):564-569. doi: 10.1016/j.clnu.2016.02.005. Epub 2016 Feb 13.
BACKGROUND & AIMS: Free fatty acids (FFAs) and their derivatives are detected by G-protein coupled receptors (GPRs) on enteroendocrine cells, with specific transporters on enterocytes. It is unknown whether acute fat exposure affects FFA sensors/transporters, and whether this relates to hormone secretion and habitual fat intake.
We studied 20 healthy participants (10M, 10F; BMI: 22 ± 1 kg/m; age: 28 ± 2 years), after an overnight fast, on 2 separate days. On the first day, duodenal biopsies were collected endoscopically before, and after, a 30-min intraduodenal (ID) infusion of 10% Intralipid, and relative transcript expression of FFA receptor 1 (FFAR1), FFA receptor 4 (FFAR4), GPR119 and the FFA transporter, cluster of differentiation-36 (CD36) was quantified from biopsies. On the second day, ID Intralipid was infused for 120-min, and plasma concentrations of cholecystokinin (CCK) and glucagon-like peptide-1 (GLP-1) evaluated. Habitual dietary intake was assessed using food frequency questionnaires (FFQs).
ID Intralipid increased expression of GPR119, but not FFAR1, FFAR4 and CD36, and stimulated CCK and GLP-1 secretion. Habitual polyunsaturated fatty acid (PUFA) consumption was negatively associated with basal GPR119 expression.
GPR119 is an early transcriptional responder to duodenal lipid in lean humans, although this response appeared reduced in individuals with high PUFA intake. These observations may have implications for downstream regulation of gut hormone secretion and appetite. This study was registered as a clinical trial with the Australia and New Zealand Clinical Trial Registry (Trial number: ACTRN12612000376842).
游离脂肪酸（FFAs）及其衍生物通过肠内分泌细胞上的 G 蛋白偶联受体（GPRs）被检测到，而特定的转运蛋白则位于肠细胞上。目前尚不清楚急性脂肪暴露是否会影响 FFA 传感器/转运蛋白，以及这是否与激素分泌和习惯性脂肪摄入有关。
我们研究了 20 名健康参与者（10 名男性，10 名女性；BMI：22±1kg/m；年龄：28±2 岁），在禁食过夜后，在 2 天内分别进行研究。在第一天，通过内窥镜在十二指肠内（ID）输注 10%Intralipid 前和输注 30 分钟后采集十二指肠活检，并从活检中定量检测游离脂肪酸受体 1（FFAR1）、游离脂肪酸受体 4（FFAR4）、GPR119 和游离脂肪酸转运蛋白，分化簇 36（CD36）的相对转录表达。在第二天，IDIntralipid 输注 120 分钟，并评估血浆胆囊收缩素（CCK）和胰高血糖素样肽-1（GLP-1）浓度。习惯性饮食摄入量通过食物频率问卷（FFQ）进行评估。
IDIntralipid 增加了 GPR119 的表达，但不增加 FFAR1、FFAR4 和 CD36 的表达，并刺激 CCK 和 GLP-1 的分泌。习惯性多不饱和脂肪酸（PUFA）的消耗与基础 GPR119 表达呈负相关。
GPR119 是瘦人十二指肠脂肪的早期转录应答物，尽管在高 PUFA 摄入个体中，这种反应似乎减少了。这些观察结果可能对肠道激素分泌和食欲的下游调节具有重要意义。本研究在澳大利亚和新西兰临床试验注册中心（注册号：ACTRN12612000376842）注册为临床试验。
