Chong Mary F-F, Fielding Barbara A, Frayn Keith N
Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford, United Kingdom.
Am J Clin Nutr. 2007 Jun;85(6):1511-20. doi: 10.1093/ajcn/85.6.1511.
A high fructose intake can lead to postprandial hypertriacylglycerolemia. The underlying mechanism is unclear.
The objective of the study was to investigate the mechanisms involved in fructose-induced hypertriacylglycerolemia and the contribution of de novo lipogenesis in an acute setting.
In a randomized, crossover study, 14 subjects were given a fructose or glucose test meal after an overnight fast. [(2)H2]Palmitate and [U(13)C]d-fructose or [U(13)C]d-glucose were added to trace the handling of dietary fats and the fate of dietary sugars in the body. Blood samples were taken before and after the meal. Respiratory exchange ratio was measured by using indirect calorimetry, and breath samples were collected.
Plasma triacylglycerol and VLDL-triacylglycerol concentrations were significantly higher (P = 0.001 for both), whereas the concentrations of insulin and [(2)H2]palmitate in nonesterified fatty acids were significantly lower after fructose than after glucose (P = 0.002 and 0.03, respectively). The respiratory exchange ratio was higher after fructose (P = 0.04); significantly (P = 0.003) more carbon from sugars was recovered in breath carbon dioxide over 6 h after fructose (30.5%) than after glucose (24.5%). At 240 min, newly synthesized fatty acids from fructose made up approximately 0.4% of circulating VLDL-triacylglycerol, whereas newly synthesized triacylglycerol-glycerol made up 38%. Newly synthesized fatty acids and triacylglycerol-glycerol from glucose contributed almost none of VLDL-triacylglycerol (P = 0.002 and 0.007 for glucose and fructose, respectively).
The lower insulin excursion after fructose may result in less activation of adipose tissue lipoprotein lipase, which led to impaired triacylglycerol clearance. The contribution of de novo lipogenesis to fructose-induced hypertriacylglycerolemia is small, but its effect on altering the partitioning of fatty acids toward esterification may be considerable.
高果糖摄入可导致餐后高甘油三酯血症。其潜在机制尚不清楚。
本研究旨在探讨果糖诱导的高甘油三酯血症的相关机制以及急性情况下从头脂肪生成的作用。
在一项随机交叉研究中，14名受试者在过夜禁食后接受果糖或葡萄糖试验餐。添加[（2）H2]棕榈酸酯和[U（13）C]d-果糖或[U（13）C]d-葡萄糖以追踪膳食脂肪的处理情况以及膳食糖在体内的去向。在餐前和餐后采集血样。使用间接量热法测量呼吸交换率，并收集呼出气体样本。
果糖餐后血浆甘油三酯和极低密度脂蛋白甘油三酯浓度显著更高（两者P均 = 0.001），而果糖餐后胰岛素浓度以及非酯化脂肪酸中[（2）H2]棕榈酸酯浓度显著低于葡萄糖餐后（分别为P = 0.002和0.03）。果糖餐后呼吸交换率更高（P = 0.04）；果糖餐后6小时呼出二氧化碳中来自糖的碳显著更多（P = 0.003），果糖餐后为30.5%，而葡萄糖餐后为24.5%。在240分钟时,果糖新合成的脂肪酸约占循环极低密度脂蛋白甘油三酯的0.4%，而新合成的甘油三酯 - 甘油占38%。葡萄糖新合成的脂肪酸和甘油三酯 - 甘油对极低密度脂蛋白甘油三酯几乎没有贡献（葡萄糖和果糖分别为P = 0.002和0.007）。
果糖摄入后胰岛素波动较小可能导致脂肪组织脂蛋白脂肪酶的激活减少，从而导致甘油三酯清除受损。从头脂肪生成对果糖诱导的高甘油三酯血症的作用较小，但其对改变脂肪酸酯化分配的影响可能相当大。
Zotero 插件