研究者们最近发现了某些膳食脂肪,如油酸(在橄榄油中发现的),更容易引起炎症的原因。实验表明,长链脂肪酸更容易促使小肠吸收促炎症细菌因子,这种因子被称为脂多糖(LPS)。该研究发表于一月刊的JLR杂志。
短链膳食脂肪(如牛奶和芝士中的脂肪)能够被小肠直接吸收并进入血液系统,而长链脂肪则要先被小肠细胞包装成被称为乳糜粒脂蛋白的大分子复合体(类似于HDL和LDL的大分子复合体)。肯塔基大学的Erik Eckhardt及其同事认为,某些经常由人类肠道内细菌携带的不良LPS复合物,可能也被组装进入乳糜粒脂蛋白。
实验证明他们的假说是正确的。他们用油酸处理培养的人类小肠细胞,能够很明显的观察到LPS与乳糜粒脂蛋白复合体共同分泌,而如果用短链的丁酸处理就不能观察到这个现象。该结果证实,LPS能明显的被血液吸收并转运,然后造成炎症基因的表达。
Eckhardt及其同事们认为,他们的发现可能为未来治疗克隆氏病和其它肠道感染疾病找到一条新路。此外,他们还指出这项研究再一次说明,在人类肠道中居住的不同种类细菌的重要性。(生物谷Bioon.com)
生物谷推荐原始出处:
Journal of Lipid Research, Vol. 50, 90-97, January 2009
Chylomicrons promote intestinal absorption of lipopolysaccharides
Sarbani Ghoshal*, Jassir Witta*, Jian Zhong*, Willem de Villiers*,, and Erik Eckhardt1,*,,
* Department of Internal Medicine, Division of Digestive Diseases and Nutrition, University of Kentucky, Lexington, KY Graduate Center for Nutritional Sciences, University of Kentucky, Lexington, KY Cardiovascular Research Center, University of Kentucky, Lexington, KY
Recent data suggest that dietary fat promotes intestinal absorption of lipopolysaccharides (LPS) from the gut microflora, which might contribute to various inflammatory disorders. The mechanism of fat-induced LPS absorption is unclear, however. Intestinal-epithelial cells can internalize LPS from the apical surface and transport LPS to the Golgi. The Golgi complex also contains newly formed chylomicrons, the lipoproteins that transport dietary long-chain fat through mesenteric lymph and blood. Because LPS has affinity for chylomicrons, we hypothesized that chylomicron formation promotes LPS absorption. In agreement with our hypothesis, we found that CaCo-2 cells released more cell-associated LPS after incubation with oleic-acid (OA), a long-chain fatty acid that induces chylomicron formation, than with butyric acid (BA), a short-chain fatty acid that does not induce chylomicron formation. Moreover, the effect of OA was blocked by the inhibitor of chylomicron formation, Pluronic L-81. We also observed that intragastric triolein (TO) gavage was followed by increased plasma LPS, whereas gavage with tributyrin (TB), or TO plus Pluronic L-81, was not. Most intestinally absorbed LPS was present on chylomicron remnants (CM-R) in the blood. Chylomicron formation also promoted transport of LPS through mesenteric lymph nodes (MLN) and the production of TNF mRNA in the MLN. Together, our data suggest that intestinal epithelial cells may release LPS on chylomicrons from cell-associated pools. Chylomicron-associated LPS may contribute to postprandial inflammatory responses or chronic diet-induced inflammation in chylomicron target tissues. |