Berkowitz Bruce A, Bissig David, Patel Priya, Bhatia Ankit, Roberts Robin
Department of Anatomy and Cell Biology, Wayne State University, Detroit, MI 48201, USA.
Mol Vis. 2012;18:372-6. Epub 2012 Feb 7.
To test the hypothesis that in dark-adapted diabetic mice subnormal manganese uptake in the outer retina can be ameliorated with exogenous 11-cis-retinal intervention.
Three groups were studied: age-matched controls and mice that had been diabetic for 3 months with and without acute, systemic 11-cis-retinal treatment administered 30 min before the manganese injection. Mice in each group were examined with manganese-enhanced magnetic resonance imaging (MEMRI) to assess central intraretinal manganese uptake and extraocular muscle manganese uptake. Bodyweights and glycated hemoglobin were determined.
Both diabetic groups had lower bodyweights and higher glycated hemoglobin levels relative to controls; no differences in these parameters between diabetic groups were noted. No substantial differences in muscle uptake were noted between any of the groups. Diabetes produced a subnormal intraretinal uptake of manganese; acute exogenous 11-cis-retinal significantly corrected only outer retinal uptake, although not to control levels.
The present results provide for the first time evidence that raises the possibility of a critical role of 11-cis-retinal, a key participant of the visual cycle, in diabetes-evoked outer retinal dysfunction.
验证以下假设，即在暗适应的糖尿病小鼠中，外视网膜锰摄取不足可通过外源性11-顺式视黄醛干预得到改善。
研究了三组：年龄匹配的对照组以及糖尿病病程3个月的小鼠，后者在注射锰前30分钟接受或未接受急性全身性11-顺式视黄醛治疗。每组小鼠均采用锰增强磁共振成像（MEMRI）检查，以评估视网膜中央锰摄取和眼外肌锰摄取。测定体重和糖化血红蛋白。
相对于对照组，两个糖尿病组的体重均较低，糖化血红蛋白水平较高；糖尿病组之间在这些参数上未发现差异。各组之间在肌肉摄取方面未发现实质性差异。糖尿病导致视网膜内锰摄取不足；急性外源性11-顺式视黄醛仅显著纠正了外视网膜摄取，尽管未恢复到对照水平。
本研究结果首次提供了证据，提示视觉循环的关键参与者11-顺式视黄醛在糖尿病诱发的外视网膜功能障碍中可能起关键作用。
