Patten Glen S, Adams Michael J, Dallimore Julie A, Rogers Paul F, Topping David L, Abeywardena Mahinda Y
CSIRO Health Sciences & Nutrition, Adelaide, South Australia 5000, Australia.
Lipids. 2005 Jan;40(1):69-79. doi: 10.1007/s11745-005-1361-9.
We have reported that dietary fish oil (FO) rich in n-3 PUFA modulates gut contractility. It was further demonstrated that the gut of spontaneously hypertensive rats (SHR) has a depressed contractility response to prostaglandins (PG) compared with normotensive Wistar-Kyoto (WKY) rats. We investigated whether feeding diets supplemented with n-3 PUFA increased gut contractility and restored the depressed prostanoid response in SHR gut. Thirteen-week-old SHR were fed diets containing fat at 5 g/100 g as coconut oil (CO), lard, canola oil containing 10% (w/w) n-3 FA as alpha-linolenic acid (1 8:3n-3), or FO (as HiDHA, 22:6n-3) for 12 wk. A control WKY group was fed 5 g/100 g CO in the diet. As confirmed, the SHR CO group had a significantly lower gut response to PGE2 and PGF2alpha compared with the WKY CO group. Feeding FO increased the maximal contraction response to acetylcholine in the ileum compared with all diets and in the colon compared with lard, and restored the depressed response to PGE2 and PGF2alpha in the ileum but not the colon of SHR. FO feeding also led to a significant increase in gut total phospholipid n-3 PUFA as DHA (22:6n-3) with lower n-6 PUFA as arachidonic acid (20:4n-6). Canola feeding led to a small increase in ileal EPA (20:5n-3) and DHA and in colonic DHA without affecting contractility. However, there was no change in ileal membrane muscarinic binding properties due to FO feeding. This report confirms that dietary FO increases muscarinic- and eicosanoid receptor-induced contractility in ileum and that the depressed prostanoid response in SHR ileum, but not colon, is restored by tissue incorporation of DHA as the active nutrient.
我们曾报道富含n-3多不饱和脂肪酸（PUFA）的膳食鱼油（FO）可调节肠道收缩性。进一步研究表明，与血压正常的Wistar-Kyoto（WKY）大鼠相比，自发性高血压大鼠（SHR）的肠道对前列腺素（PG）的收缩反应降低。我们研究了补充n-3 PUFA的饮食是否能增加SHR肠道的收缩性，并恢复其肠道中降低的类前列腺素反应。给13周龄的SHR喂食含5 g/100 g脂肪的饮食，脂肪种类分别为椰子油（CO）、猪油、含10%（w/w）n-3脂肪酸（α-亚麻酸，18:3n-3）的菜籽油或鱼油（高二十二碳六烯酸，22:6n-3），持续12周。一个WKY对照小组喂食含5 g/100 g CO的饮食。如预期所料，与WKY CO组相比，SHR CO组对前列腺素E2和前列腺素F2α的肠道反应显著降低。与所有饮食组相比，喂食鱼油可增加回肠对乙酰胆碱的最大收缩反应，与猪油组相比，喂食鱼油还可增加结肠对乙酰胆碱的最大收缩反应，并且恢复了SHR回肠而非结肠中对前列腺素E2和前列腺素F2α降低的反应。喂食鱼油还导致肠道总磷脂中n-3 PUFA（二十二碳六烯酸，22:6n-3）显著增加，同时n-6 PUFA（花生四烯酸，20:4n-6）降低。喂食菜籽油使回肠中二十碳五烯酸（20:5n-3）和二十二碳六烯酸以及结肠中二十二碳六烯酸略有增加，但不影响收缩性。然而，喂食鱼油并未改变回肠膜毒蕈碱结合特性。本报告证实，膳食鱼油可增加回肠中由毒蕈碱和类花生酸受体诱导的收缩性，并且通过组织摄取作为活性营养素的二十二碳六烯酸可恢复SHR回肠而非结肠中降低的类前列腺素反应。
