FAT FEEDING INCREASES SIZE, BUT NOT NUMBER, OF CHYLOMICRONS PRODUCED BY SMALL-INTESTINE
FAT FEEDING INCREASES SIZE, BUT NOT NUMBER, OF CHYLOMICRONS PRODUCED BY SMALL-INTESTINE
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DOI：
10.1152/ajpgi.1990.259.5.g709
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发表时间：
1990-11-01
影响因子：
--
通讯作者：
TSO, P
中科院分区：
文献类型：
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作者：
HAYASHI, H;FUJIMOTO, K;TSO, P
为了研究膳食甘油三酯（TG）对大鼠淋巴载脂蛋白B （apo B）转运的调节作用，以3 ml/h的速度向淋巴瘘大鼠十二指肠内注射含40 .mu的脂质乳剂8 h。mol TG标记甘油[9,103H(N)]三油酸，7.8 .mu。蛋磷脂酰胆碱57 μ。添加或不添加1mg /h Pluronic L81 （L81）的磷酸缓冲盐水中的牛磺胆酸钠。已知L81通过抑制乳糜微粒（CM）的形成来阻止肠内脂质运输。L81的这种作用可以通过盐水输注取代L81而迅速逆转。在对照大鼠中（不添加L81），在脂质输注期间，与禁食相比，在整个淋巴、CM或极低密度脂蛋白（VLDL）部分中分泌的载脂蛋白B的量没有显着变化。与空腹相比，L81 +脂质或生理盐水输注实验大鼠淋巴载脂蛋白B输出量无明显变化。淋巴载脂蛋白B输出数据也得到了[3H]亮氨酸掺入研究的支持。综上所述，这些数据表明，吸收生理负荷的脂质进入淋巴并不影响粘膜中载脂蛋白B的合成或淋巴中载脂蛋白B的分泌。此外，L81的作用可能不是通过抑制肠道载脂蛋白B的产生，因为载脂蛋白B的分泌不受L81存在的影响。本研究还表明，在禁食或活跃的脂质摄取和运输期间，小肠制造的CM颗粒数量保持相对恒定。在活性脂质吸收过程中，肠细胞不是增加CM的数量，而是扩大CM颗粒的大小。最后，小肠合成和分泌的VLDL颗粒的数量和TG含量在禁食和活跃脂质吸收期间似乎也保持相对恒定。
To test the regulatory effect of dietary triglyceride (TG) on rat lymphatic apoliopoprotein B (apo B) transport, lymph-fistula rats were infused intraduodenally for 8 h at 3 ml/h with a lipid emulsion containing 40 .mu.mol TG labeled with glycerol [9,103H(N)]triolein, 7.8 .mu.mol egg phosphatidylcholine, and 57 .mu.mol 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 added to 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.