Holt P R, Dominguez A A
Am J Physiol. 1980 May;238(5):G453-7. doi: 10.1152/ajpgi.1980.238.5.G453.
To estimate intestinal very low-density lipoprotein (VLDL) contribution to the circulating plasma triglyceride (TG) pool, mesenteric, hepatic, and total TG production rates were measured in mesenteric lymph-cannulated male rats after Triton WR-1339 blockage of systemic VLDL metabolism. The intestinal contribution (4.92 +/- 0.5 mg TG/h) was calculated to be 19% of total TG production rate. Triton WR-1339 administration caused profound hyperlipoproteinemia but did not alter total lymph TG or VLDL apoprotein output. The percent of lymph VLDL apoprotein present as apo A-I and apo A-IV fell dramatically after Triton with a concomitant increase in apo E and apo C peptides. Studies in this Triton-treated rat model suggest that the intestinal contribution to systemic TG formation is small but that changes in circulating apolipoproteins may alter the composition of intestinal VLDL.
为了评估肠道极低密度脂蛋白（VLDL）对循环血浆甘油三酯（TG）池的贡献，在通过Triton WR-1339阻断全身VLDL代谢后，对肠系膜淋巴管插管的雄性大鼠测量了肠系膜、肝脏和总TG生成率。肠道的贡献（4.92±0.5mg TG/小时）经计算占总TG生成率的19%。给予Triton WR-1339导致严重的高脂蛋白血症，但未改变总淋巴TG或VLDL载脂蛋白输出。Triton处理后，淋巴VLDL载脂蛋白中以载脂蛋白A-I和载脂蛋白A-IV形式存在的百分比急剧下降，同时载脂蛋白E和载脂蛋白C肽增加。在这个经Triton处理的大鼠模型中的研究表明，肠道对全身TG形成的贡献很小，但循环载脂蛋白的变化可能会改变肠道VLDL的组成。
