Kalogeris T J, Tsuchiya T, Fukagawa K, Wolf R, Tso P
Department of Physiology and Biophysics, Louisiana State University Medical Center, Shreveport 71130, USA.
Am J Physiol. 1996 Feb;270(2 Pt 1):G277-86. doi: 10.1152/ajpgi.1996.270.2.G277.
Biosynthesis of apolipoprotein A-IV (apo A-IV) is stimulated by dietary lipid, but the precise mechanisms involved are not clearly understood. Using an intestinally infused rat model, we compared the effect of delivery of lipid into different intestinal sites on mucosal synthesis of apo A-IV in the jejunum and ileum to determine 1) the effect of lipid delivered to one region of the intestine on apo A-IV synthesis in another region of the gut, and 2) whether any such effect is dependent on the presence of lipid in the latter region. Duodenal infusion of triolein emulsion (40 mumol/h) increased jejunal apo A-IV synthesis and mRNA levels by two- to threefold but had no effect on ileal apo A-IV synthesis or mRNA abundance. Ileal infusion of lipid emulsion containing monoolein (20 mumol/h) + oleic acid (40 mumol/h) stimulated apo A-IV synthesis in both ileum and proximal jejunum. Retrograde (orad) transport of ileally infused lipid was not a likely explanation for the ileal effect on jejunal apo A-IV synthesis, because there was negligible luminal and mucosal recovery of [14C]oleic acid in the jejunum after ileal infusion. Total bile diversion did not block the effect of ileal lipid on jejunal apo A-IV synthesis. Ileal, but not duodenal, lipid infusion stimulated apo A-IV synthesis in a jejunal Thiry-Vella fistula, and perfusion of an ileal Thiry-Vella fistula marginally stimulated proximal jejunal apo A-IV synthesis. Thus administration of lipid to the distal gut produces an increase in mucosal synthesis of apo A-IV in both proximal and distal gut. This effect appears to be independent of direct jejunal presence of lipid, suggesting that lipid in the distal intestine may elicit a signal capable of stimulating jejunal synthesis of apo A-IV.
载脂蛋白A-IV(apo A-IV)的生物合成受膳食脂质刺激,但其中的确切机制尚不清楚。我们使用肠内灌注大鼠模型,比较了将脂质输送到不同肠道部位对空肠和回肠黏膜apo A-IV合成的影响,以确定:1)将脂质输送到肠道一个区域对肠道另一区域apo A-IV合成的影响;2)这种影响是否依赖于后一区域脂质的存在。十二指肠灌注三油酸甘油酯乳剂(40 μmol/h)可使空肠apo A-IV合成及mRNA水平增加2至3倍,但对回肠apo A-IV合成或mRNA丰度无影响。回肠灌注含单油酸甘油酯(20 μmol/h)+油酸(40 μmol/h)的脂质乳剂可刺激回肠和空肠近端的apo A-IV合成。回肠灌注脂质向空肠的逆行(向口腔方向)转运不太可能是回肠对空肠apo A-IV合成产生影响的原因,因为回肠灌注后空肠腔内和黏膜中[14C]油酸的回收率可忽略不计。完全胆汁分流并未阻断回肠脂质对空肠apo A-IV合成的影响。回肠而非十二指肠脂质灌注可刺激空肠Thiry-Vella瘘管中的apo A-IV合成,回肠Thiry-Vella瘘管的灌注略微刺激空肠近端的apo A-IV合成。因此,向远端肠道给予脂质会使近端和远端肠道的黏膜apo A-IV合成增加。这种作用似乎不依赖于脂质在空肠中的直接存在,提示远端肠道中的脂质可能引发一种能够刺激空肠apo A-IV合成的信号。