Heath Richard B, Karpe Fredrik, Milne Ross W, Burdge Graham C, Wootton Stephen A, Frayn Keith N
Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford OX3 7LJ, UK.
Am J Physiol Endocrinol Metab. 2007 Mar;292(3):E732-9. doi: 10.1152/ajpendo.00409.2006. Epub 2006 Nov 7.
Exaggerated postprandial lipemia is associated with coronary heart disease and type II diabetes, yet few studies have examined the effect of sequential meals on lipoprotein metabolism. We have used 13C-labeled fatty acids to trace the incorporation of fatty acid derived from a meal into apolipoprotein B-100 (apoB-100)-containing lipoproteins and plasma nonesterified fatty acids (NEFA) following two consecutive meals. Healthy volunteers (n=8) were given breakfast labeled with [1-(13)C]palmitic acid, eicosapentaenoic acid, and docosahexaenoic acid, followed 5 h later by lunch containing [1-(13)C]oleic acid. Blood samples were taken over a 9-h period. ApoB-100-containing lipoproteins were isolated by immunoaffinity chromatography. Chylomicron-triacylglycerol (TG) concentrations peaked at 195 min following breakfast but at 75 min following lunch (P<0.001). VLDL-TG concentrations, in contrast, rose to a broad peak after breakfast and then fell steadily after lunch. Breakfast markers followed chylomicron-TG concentrations and appeared in plasma NEFA with a similar profile, whereas [1-(13)C]oleic acid peaked 2 h after lunch in plasma TG and NEFA. Breakfast markers appeared steadily in VLDL, peaking 1-3 h after lunch, whereas [1-(13)C]oleic acid was still accumulating in VLDL at 9 h. Around 17% of VLDL-TG originated from recent dietary fat 5 h after breakfast, and around 40% at the end of the experiment. We conclude that there is rapid flux of fatty acids from the diet into endogenous pools. Further study of these processes may open up new targets for intervention to reduce VLDL-TG concentrations and postprandial lipemia.
餐后血脂过高与冠心病和II型糖尿病有关，但很少有研究探讨连续进餐对脂蛋白代谢的影响。我们使用13C标记的脂肪酸来追踪一餐中衍生的脂肪酸在连续两餐后掺入含载脂蛋白B-100（apoB-100）的脂蛋白和血浆非酯化脂肪酸（NEFA）中的情况。健康志愿者（n = 8）先食用标记有[1-(13)C]棕榈酸、二十碳五烯酸和二十二碳六烯酸的早餐，5小时后再食用含[1-(13)C]油酸的午餐。在9小时内采集血样。通过免疫亲和色谱法分离含apoB-100的脂蛋白。餐后乳糜微粒三酰甘油（TG）浓度在早餐后195分钟达到峰值，但在午餐后75分钟达到峰值（P<0.001）。相比之下，极低密度脂蛋白（VLDL）-TG浓度在早餐后升至一个较宽的峰值，然后在午餐后稳步下降。早餐标记物随乳糜微粒-TG浓度变化，并以类似的模式出现在血浆NEFA中，而[1-(13)C]油酸在午餐后2小时在血浆TG和NEFA中达到峰值。早餐标记物稳定地出现在VLDL中，在午餐后1 - 3小时达到峰值，而[1-(13)C]油酸在9小时时仍在VLDL中积累。早餐后5小时，约17%的VLDL-TG源自近期饮食脂肪，在实验结束时约为40%。我们得出结论，脂肪酸从饮食中快速流入内源性库。对这些过程的进一步研究可能会为降低VLDL-TG浓度和餐后血脂过高开辟新的干预靶点。
