Diabetic retinopathy is thought to be trigger by glucose- induced oxidative stress which leads to an increase of the mitochondrial permeability through opening the permeability transition pore (MTP). In several cell types, hexokinases interact with the mitochondria regulating MTP opening, avoiding cytochrome c release. We studied HK I mitochondrial proportion in control and streptozotocin-induced diabetic rat retinas. In the normal retina, 50% of HK I was linked to mitochondria, proportion that did not change up to 60 days of diabetes. Mitochondria from normal and diabetic rat retinas showed a limited swelling, and similar cytochrome c levels. G-6-P and glycogen content increased 3-6-fold in diabetic rat retinas, while lactate content did not vary. Results suggest that mitochondrial bound HK produce G-6-P and drove it to glycogen synthesis, controlling ROS production and lactate toxicity.

中文翻译：

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正常和链脲佐菌素糖尿病大鼠视网膜中的线粒体结合己糖激酶 I 型

糖尿病视网膜病变被认为是由葡萄糖诱导的氧化应激引发的，氧化应激通过打开通透性转换孔 (MTP) 导致线粒体通透性增加。在几种细胞类型中，己糖激酶与调节 MTP 开放的线粒体相互作用，避免细胞色素 c 释放。我们研究了对照和链脲佐菌素诱导的糖尿病大鼠视网膜中的 HK I 线粒体比例。在正常视网膜中，50% 的 HK I 与线粒体有关，这一比例在糖尿病患者 60 天后没有变化。来自正常和糖尿病大鼠视网膜的线粒体显示出有限的肿胀和相似的细胞色素 c 水平。G-6-P 和糖原含量在糖尿病大鼠视网膜中增加了 3-6 倍，而乳酸含量没有变化。结果表明，线粒体结合的 HK 产生 G-6-P 并驱动它合成糖原，