Hayashi H, Fujimoto K, Cardelli J A, Nutting D F, Bergstedt S, Tso P
Department of Physiology, Louisiana State University Medical Center, Shreveport 71130.
Am J Physiol. 1990 Nov;259(5 Pt 1):G709-19. doi: 10.1152/ajpgi.1990.259.5.G709.
To test the regulatory effect of dietary triglyceride (TG) on rat lymphatic apolipoprotein B (apo B) transport, lymph-fistula rats were infused intraduodenally for 8 h at 3 ml/h with a lipid emulsion containing 40 mumol TG labeled with glycerol [9,10-3H(N)]triolein, 7.8 mumol egg phosphatidylcholine, and 57 mumol sodium taurocholate in phosphate-buffered saline with or without 1 mg/h Pluronic L81 (L81). L81 is known to prevent lipid transport in the intestine by inhibiting the formation of chylomicrons (CM). This action of L81 is quickly reversible by merely replacing L81 infusion by saline infusion. In the control rats (without L81 added to the infusate), the amount of apo B secreted in either whole lymph, CM, or the very-low-density lipoprotein (VLDL) fractions did not change significantly during lipid infusion compared with fasting. Compared with the fasting, the apo B output in lymph during L81 plus lipid or saline infusion in the experimental rats did not change significantly. The lymphatic apo B output data were also supported by the incorporation studies using [3H]leucine. In summary, these data demonstrate that the absorption of a physiological load of lipid into lymph does not affect the apo B synthesis in the mucosa or the secretion of apo B in lymph. Furthermore, the action of L81 is probably not by inhibiting intestinal apo B production because apo B secretion was not affected by the presence of L81. This study also demonstrates that the number of CM particles made by the small intestine remains relatively constant during fasting or active lipid uptake and transport. During active lipid absorption, instead of increasing the number of CM, the enterocytes expand the size of the CM particles. Lastly, the number and TG content of VLDL particles synthesized and secreted by the small intestine also seems to remain relatively constant during fasting and active lipid absorption.
为了测试膳食甘油三酯（TG）对大鼠淋巴载脂蛋白B（apo B）转运的调节作用，对淋巴瘘大鼠以3 ml/h的速度经十二指肠内输注含40 μmol甘油[9,10-3H(N)]三油酸甘油酯标记的TG、7.8 μmol蛋黄卵磷脂和57 μmol牛磺胆酸钠的脂质乳剂，持续8小时，输注液中添加或不添加1 mg/h的普朗尼克L81（L81）。已知L81通过抑制乳糜微粒（CM）的形成来阻止脂质在肠道中的转运。仅通过将L81输注替换为生理盐水输注，L81的这种作用即可迅速逆转。在对照大鼠（输注液中未添加L81）中，与禁食相比，脂质输注期间全淋巴、CM或极低密度脂蛋白（VLDL）组分中分泌的apo B量没有显著变化。与禁食相比，实验大鼠在L81加脂质或生理盐水输注期间淋巴中apo B的输出没有显著变化。使用[3H]亮氨酸的掺入研究也支持了淋巴apo B输出数据。总之，这些数据表明，生理负荷的脂质吸收到淋巴中不会影响黏膜中apo B的合成或淋巴中apo B的分泌。此外，L81的作用可能不是通过抑制肠道apo B的产生，因为L81的存在并不影响apo B的分泌。这项研究还表明，在禁食或活跃的脂质摄取和转运过程中，小肠产生的CM颗粒数量保持相对恒定。在活跃的脂质吸收过程中，肠细胞不是增加CM的数量，而是扩大CM颗粒的大小。最后，在禁食和活跃的脂质吸收过程中，小肠合成和分泌VLDL颗粒的数量和TG含量似乎也保持相对恒定。
