Instituto de Biología Celular, Histología y Embriología, Facultad de Ciencias Médicas, INICSA (CONICET-Universidad Nacional de Córdoba), Córdoba, Argentina.
Lipids Health Dis. 2019 May 15;18(1):114. doi: 10.1186/s12944-019-1049-9.
Vision disorders are one of the most serious complications of diabetes mellitus (DM) affecting the quality of life of patients and eventually cause blindness. The ocular lesions in diabetes mellitus are located mainly in the blood vessels and retina layers. Different retina lesions could be grouped under the umbrella term of diabetic retinopathies (DMRP).We propose that one of the main causes in the etiopathogenesis of the DMRP consists of a progressive loss of the selective permeability of blood retinal barriers (BRB). The loss of selective permeability of blood retinal barriers will cause a progressive autoimmune process. Prolonged autoimmune injures in the retinal territory will triggers and maintains a low-grade chronic inflammation process, microvascular alterations, glial proliferation and subsequent fibrosis and worse, progressive apoptosis of the photoreceptor neurons.Patients with long-standing DM disturbances in retinal BRBs suffer of alterations in the enzymatic pathways of polyunsaturated fatty acids (PUFAs), increase release of free radicals and pro-inflammatory molecules and subsequently incremented levels of vascular endothelial growth factor. These facts can produce retinal edema and photoreceptor apoptosis.Experimental, clinical and epidemiological evidences showing that adequate metabolic and alimentary controls and constant practices of healthy life may avoid, retard or make less severe the appearance of DMRP. Considering the high demand for PUFAs ω3 by photoreceptor complexes of the retina, it seems advisable to take fish oil supplements (2 g per day). The cellular, subcellular and molecular basis of the propositions exposed above is developed in this article.Synthesizer drawings the most relevant findings of the ultrastructural pathology, as well as the main metabolic pathways of the PUFAs involved in balance and disbalanced conditions are provided.
视力障碍是糖尿病（DM）最严重的并发症之一，影响患者的生活质量，最终导致失明。糖尿病的眼部病变主要位于血管和视网膜层。不同的视网膜病变可以归为糖尿病性视网膜病变（DMRP）这一总称。我们认为，DMRP 的发病机制之一主要是血视网膜屏障（BRB）的选择性通透性逐渐丧失。BRB 的选择性通透性丧失会导致进行性自身免疫过程。视网膜区域的持续性自身免疫损伤会引发和维持低度慢性炎症过程、微血管改变、胶质细胞增生以及随后的纤维化，更糟糕的是，感光细胞神经元的进行性凋亡。患有长期 DM 视网膜 BRB 障碍的患者，其多不饱和脂肪酸（PUFAs）的酶途径会发生改变，自由基和促炎分子的释放增加，随后血管内皮生长因子水平升高。这些因素会导致视网膜水肿和感光细胞凋亡。实验、临床和流行病学证据表明，适当的代谢和饮食控制以及健康生活的持续实践可以预防、延缓或减轻 DMRP 的发生。鉴于感光细胞复合体对 PUFAs ω3 的高需求，似乎可以服用鱼油补充剂（每天 2 克）。本文阐述了上述观点的细胞、亚细胞和分子基础。综合器绘制了超微结构病理学的最相关发现，以及涉及平衡和失衡状态的 PUFAs 的主要代谢途径。
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