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ω3 匮乏型大鼠的代谢综合征。六、肠道磷脂饱和及单不饱和脂肪酸。

The metabolic syndrome of omega3-depleted rats. VI. Intestinal phospholipid saturated and monodesaturated fatty acids.

机构信息

Laboratory of Experimental Surgery, Université Libre de Bruxelles, B-1070 Brussels, Belgium.

出版信息

Int J Mol Med. 2010 Jan;25(1):171-81.

PMID:19956917
Abstract

Exposure of normal rats for 3-7 months to an omega3-deprived diet and subsequent exposure to an omega3-enriched diet were recently proposed as a model to study the metabolic consequences of alteration in the dietary supply of omega3 PUFA and their time course. The same animal model was used in the present study, which aimed at characterizing the pattern of saturated and monodesaturated fatty acids in the phospholipids of the duodenum, jejunum, caecum and colon. With one exception (C18:0), the weight content of these fatty acids was lower in the proximal than distal intestinal segments, a situation possibly accounted for by the generation of short-chain fatty acids by the colonic flora and the resulting synthesis of longer fatty acids n colonocytes. The relative weight content of the 8 fatty acids under consideration (C14:0, C16:0, C16:1omega7, C18:0, C18:1omega9, C20:0, C22:0 and C24:0) was higher in the phospholipids of omega3-deprived rats, as compared to control animals. Exposure of either the control animals or omega3-deprived rats for 2-4 weeks to diets containing twice more lipids than the control or omega3-deprived diet given theretofore further increased, as a rule, the relative content of phospholipids in the saturated or monodesaturated fatty acids, such an increase being much more pronounced in the proximal segments of the intestinal tract than in the distal ones. A significant inverse correlation between the phospholipid content in C22:6omega3 and saturated and monodesaturated fatty acids was only observed in the caecum and colon.

摘要

正常大鼠暴露于 omega3 缺乏饮食 3-7 个月,随后暴露于 omega3 丰富饮食中,最近被提议作为研究饮食中 omega3PUFA 供应改变及其时间过程对代谢影响的模型。本研究采用了相同的动物模型,旨在描述十二指肠、空肠、盲肠和结肠磷脂中饱和和单不饱和脂肪酸的模式。除了一个例外(C18:0),这些脂肪酸的重量含量在近端肠段比远端肠段低,这种情况可能是由于结肠菌群产生短链脂肪酸,以及结肠细胞中长链脂肪酸的合成造成的。在所考虑的 8 种脂肪酸(C14:0、C16:0、C16:1omega7、C18:0、C18:1omega9、C20:0、C22:0 和 C24:0)中,与对照组相比,omega3 缺乏组的磷脂中相对重量含量更高。暴露于两倍于对照组或 omega3 缺乏饮食的饮食中 2-4 周的对照组或 omega3 缺乏大鼠,通常会进一步增加饱和或单不饱和脂肪酸的磷脂相对含量,这种增加在肠道的近端比远端更为明显。只有在盲肠和结肠中才观察到 C22:6omega3 与饱和和单不饱和脂肪酸的磷脂含量之间存在显著的负相关。

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