Kalogeris T J, Fukagawa K, Tso P
Department of Physiology, Louisiana State University School of Medicine, Shreveport 71130.
J Lipid Res. 1994 Jul;35(7):1141-51.
Factors regulating the intestinal synthesis and secretion of apoA-IV are incompletely understood. Although it is known that apoA-IV is stimulated by dietary lipid, it is not known whether graded doses of triglyceride elicit graded responses in apoA-IV synthesis and secretion. We used the chronic intestinal lymph-fistula rat to examine the effect of graded levels of intestinal triglyceride transport on secretion of apoA-IV into lymph and synthesis of apoA-IV in various regions of intestine. Rats were implanted with chronic duodenal and intestinal lymph duct cannulas and infused with lipid emulsions containing 5, 10, 20, 40, 80 mumol triolein (including [3H]triolein, 1.2 microCi), 8.7 mumol phosphatidylcholine, and 57 mumol sodium taurocholate in 3 ml phosphate-buffered saline (pH 6.4) at ml/h for 8 h. Lymph samples were collected for 1 h prior to and at 2, 4, 5, 6, 7, and 8 h after the start of lipid infusion. Lymphatic output of triglyceride, phospholipid, and apoA-IV was measured. Steady-state (8 h) content of radioactive lipid was also measured in the lumen and the wall of the gut. In separate studies rats were given infusions of either 5% glucose in saline ("fasting") or triolein emulsion (10, 20, 40, 80 mumol/h) for 8 h after which incorporation of [3H]leucine into apoA-IV in isolated, in situ loops of duodenum, proximal jejunum, mid-distal jejunum, and terminal ileum was measured. Lipid output increased dose-dependently in response to triolein infusion, with steady-state lipid transport achieved by 5 h after start of lipid infusion. Total recovery of 3H-labeled lipid was similar for all triolein doses. Increase in lymphatic apoA-IV output lagged that of triglyceride by 3-4 h, but by 8 h showed graded increases with triolein dose. ApoA-IV synthesis (apoA-IV radioactivity immunoprecipitated by an apoA-IV monospecific antibody and expressed as % of trichloroacetic acid-precipitable [3H]leucine radioactivity) in the duodenum and proximal jejunum showed a 2-fold increase (compared with fasting) in response to 10 mumol triolein/h, but no further increase at higher doses. However, apoA-IV synthesis in mid to distal jejunum increased dose-dependently.(ABSTRACT TRUNCATED AT 400 WORDS)
调节载脂蛋白A-IV在肠道合成与分泌的因素尚未完全明确。尽管已知膳食脂质可刺激载脂蛋白A-IV的产生，但尚不清楚不同剂量的甘油三酯是否会引起载脂蛋白A-IV合成与分泌的相应变化。我们利用慢性肠淋巴瘘大鼠，研究肠道甘油三酯转运水平的变化对载脂蛋白A-IV分泌入淋巴以及在肠道不同区域合成的影响。给大鼠植入慢性十二指肠和肠淋巴管插管，并以每小时1毫升的速度，在3毫升磷酸盐缓冲液（pH 6.4）中注入含5、10、20、40、80微摩尔三油精（包括[3H]三油精，1.2微居里）、8.7微摩尔磷脂酰胆碱和57微摩尔牛磺胆酸钠的脂质乳剂，持续8小时。在脂质注入开始前1小时以及注入后2、4、5、6、7和8小时收集淋巴样本。测量甘油三酯、磷脂和载脂蛋白A-IV的淋巴输出量。同时测量肠道管腔和肠壁中放射性脂质的稳态（8小时）含量。在另外的研究中，给大鼠分别注入生理盐水加5%葡萄糖（“禁食”状态）或三油精乳剂（10、20、40、80微摩尔/小时），持续8小时，之后测量[3H]亮氨酸在分离的十二指肠、空肠近端、空肠中远端和回肠末端原位肠袢中掺入载脂蛋白A-IV的情况。随着三油精注入，脂质输出呈剂量依赖性增加，脂质注入开始后5小时达到稳态脂质转运。所有三油精剂量下3H标记脂质的总回收率相似。载脂蛋白A-IV淋巴输出量的增加比甘油三酯滞后3 - 4小时，但到8小时时，随着三油精剂量增加呈现相应增加。十二指肠和空肠近端中载脂蛋白A-IV的合成（用载脂蛋白A-IV单特异性抗体免疫沉淀的载脂蛋白A-IV放射性，并表示为三氯乙酸可沉淀的[3H]亮氨酸放射性的百分比）在每小时注入10微摩尔三油精时比“禁食”状态增加了2倍，但在更高剂量时没有进一步增加。然而，空肠中远端载脂蛋白A-IV的合成呈剂量依赖性增加。（摘要截选至400字）
