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ω-3 多不饱和脂肪酸补充剂在糖尿病周围神经病变中的作用。

A role for omega-3 polyunsaturated fatty acid supplements in diabetic neuropathy.

机构信息

Department of Anatomy and Cell Biology, The University of Melbourne, Victoria, Australia.

出版信息

Invest Ophthalmol Vis Sci. 2010 Mar;51(3):1755-64. doi: 10.1167/iovs.09-3792. Epub 2009 Nov 11.

DOI:10.1167/iovs.09-3792
PMID:19907026
Abstract

PURPOSE

Diabetes results in an insulin-related disorder of lipid metabolism that reduces production of long-chain polyunsaturated fatty acids (PUFAs; e.g., docosahexanoic acid, DHA). This study considers the role that this lipid change has on retinal function.

METHODS

From conception, rats (n = 56) were fed diets either balanced (n = 32) in PUFAs or deficient in omega-3 (n = 24). Half were assigned to control (n = 28) or streptozotocin (STZ: n = 28) treatment at 7 weeks of age. Key metabolic indices were assayed at 19 weeks, and retinal function was determined by electroretinogram (ERG) at 20 weeks. Retinal anatomy and lipid assays of 20-week-old animals were used to identify structural changes and tissue PUFA content.

RESULTS

The systemic indices of diabetic rats were not affected by diet. Lipid composition of retinal membranes reflected the dietary manipulation, and diabetes amplified some fatty acid changes consistent with reduced desaturase activity. Diabetes produced significant reduction in rod function (-33%) only in the absence of fish oil, whereas cone responses (-46%) and inner retinal oscillatory potentials (-47%) showed either no effect of diet or a partial diet effect with a significant diabetes effect. Anatomic analysis revealed no disorder in the retinal neurons, although changes in the Müller glia were noted in diabetes, regardless of diet.

CONCLUSIONS

A diet balanced in long-chain PUFAs modifies retinal lipid membranes in diabetes and prevents rod dysfunction. Dietary modification was not found in the cone or glial response but a partial improvement was evident in the OPs, most likely secondary to the larger photoreceptor output.

摘要

目的

糖尿病导致胰岛素相关的脂质代谢紊乱,减少长链多不饱和脂肪酸(PUFA;例如二十二碳六烯酸,DHA)的产生。本研究探讨了这种脂质变化对视网膜功能的影响。

方法

从受孕开始,将大鼠(n=56)分为两组,分别喂食富含或缺乏ω-3 的平衡饮食(n=32)。其中一半在 7 周龄时被分配到对照组(n=28)或链脲佐菌素(STZ:n=28)处理组。19 周时检测关键代谢指标,20 周时用电视网膜电图(ERG)测定视网膜功能。20 周龄动物的视网膜解剖和脂质分析用于确定结构变化和组织 PUFA 含量。

结果

糖尿病大鼠的系统代谢指数不受饮食影响。视网膜膜的脂质组成反映了饮食处理,糖尿病加剧了一些与脱饱和酶活性降低一致的脂肪酸变化。糖尿病仅在缺乏鱼油的情况下显著降低了杆状细胞功能(-33%),而锥体反应(-46%)和内视网膜振荡电位(-47%)则不受饮食影响或有部分饮食影响,但糖尿病有显著影响。尽管在糖尿病中观察到了 Müller 胶质细胞的变化,但神经节细胞的形态学分析并未显示出任何异常,无论是否存在饮食。

结论

富含长链多不饱和脂肪酸的饮食可以改变糖尿病中的视网膜脂质膜,并预防杆状细胞功能障碍。在锥体或胶质反应中没有发现饮食改变,但在 OPs 中则存在部分改善,这可能是由于更大的光感受器输出所致。

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