饮食中omega-3脂肪酸和胆固醇改变糖尿病大鼠肠刷缘和微粒体膜的去饱和酶活性和脂肪酰基成分。

M Keelan, A B Thomson, M L Garg, E Wierzbicki, A A Wierzbicki, M T Clandinin
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引用次数: 0

摘要

糖尿病相关的肠道营养摄取的变化可通过膳食脂质类型的等热量改变而改变,并与肠刷状缘膜磷脂和脂肪酰基含量的改变有关。我们希望验证一种假设,即饮食和糖尿病相关的刷状边界膜磷脂脂肪酸的变化是由于肠细胞微粒体δ 5、δ 6和δ 9去饱和酶活性的改变。将成年雌性Wistar大鼠分为两组。在一半的动物中,注射链脲佐菌素产生了糖尿病,另一半动物作为非糖尿病对照组。两组均饲喂饲料两周,然后随机选择四种半合成饲料中的一种喂养两周:低胆固醇牛油(BT)、高胆固醇牛油(BTC)、低胆固醇鱼油(FO)或高胆固醇鱼油(FOC)。饲喂高胆固醇饲料可提高非糖尿病对照组大鼠空肠细胞微体膜δ -5和δ -9去饱和酶活性,糖尿病大鼠饲喂鱼油可提高δ -5去饱和酶活性,对照组和糖尿病大鼠饲喂鱼油可提高δ -5和δ -6去饱和酶的回肠活性。膳食脂肪酸、胆固醇和糖尿病并没有引起BBM磷脂酰胆碱或磷脂酰乙醇胺中脂肪酸含量的变化,这些变化是由δ -5 (20:4 ω -6和20:5 ω - 3)、δ -6 (18:3 ω -6和18:4 ω - 3)或δ -9去饱和酶(18:1 ω -9和16:1 ω - 7)的变化所引起的。-6和-9去饱和酶受膳食脂肪酸、胆固醇或糖尿病的独立影响;2)饮食脂肪酸、胆固醇和糖尿病的变化与刷状膜磷脂酰胆碱和磷脂酰乙醇胺的脂肪酰基成分的变化有关,但这些脂肪酰基的变化不能用微粒体去饱和酶活性的变化来解释。因此,肠刷状边界膜和肠细胞微粒体去饱和酶能够适应饮食脂质或糖尿病的变化,但这两种变化并不一定是因果相关的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Dietary omega-3 fatty acids and cholesterol modify desaturase activities and fatty acyl constituents of rat intestinal brush border and microsomal membranes of diabetic rats.

The diabetes-associated changes in intestinal uptake of nutrients are modified by isocaloric alterations in the type of dietary lipids, and is associated with alterations in the phospholipid and fatty acyl content of the intestinal brush border membrane. We wished to test the hypothesis that diet- and diabetes-associated changes in brush border membrane phospholipid fatty acids are due to alterations in the activity of enterocyte microsomal delta-5, delta-6 and delta-9 desaturases. Adult female Wistar rats were divided into two groups. In half of the animals, diabetes was produced with the injection of streptozotocin, and the other half of the animals served as nondiabetic controls. Both groups were raised on chow for two weeks and were then randomized to one of four semisynthetic diets for two weeks: beef tallow low in cholesterol (BT), beef tallow high in cholesterol (BTC), fish oil low in cholesterol (FO), or fish oil high in cholesterol (FOC). Feeding a high cholesterol diet increased the activity of jejunal enterocyte microsomal membrane activity of delta-5 and delta-9-desaturases when fed with FO in non-diabetic control rats, increased delta-5-desaturase in diabetic rats fed FO, and increased the ileal activity of delta-5 and delta-6-desaturases in control and diabetic animals fed FO. Dietary fatty acids, cholesterol and diabetes did not produce the changes in the amount of fatty acids in BBM phosphatidylcholine or phosphatidylethanolamine expected from the measured alterations in delta-5 (20:4 omega 6 and 20:5 omega 3), in delta-6 (18:3 omega 6 and 18:4 omega 3), or in delta-9 desaturase (18:1 omega 9 and 16:1 omega 7). In summary, 1) the activities of enterocyte microsomal membrane delta-5, delta-6 and delta-9-desaturases are independently influenced by dietary fatty acids or cholesterol, or by diabetes; 2) changes in dietary fatty acids, cholesterol and diabetes are associated with alterations in the fatty acyl constituents of brush border membrane phosphatidylcholine and phosphatidylethanolamine, but these fatty acyl changes are not explained on the basis of variations in the activities of the microsomal desaturases. Thus, the intestinal brush border membrane and the enterocyte microsomal desaturases are capable of adapting in response to changes in dietary lipids or diabetes, but the two alterations are not necessarily causally interrelated.

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