Boot-Handford R, Heath H
Metabolism. 1980 Dec;29(12):1247-52. doi: 10.1016/0026-0495(80)90153-5.
In order to determine whether the fructose moiety of sucrose or the lack of some factor essential for the integrity of the microvascular system was responsible for the development of sucrose retinopathy in the rat, a series of diets containing possible sources of such a factor and/or fructose was tested over a 6-mo period. Examination of the isolated rat retinal vascular systems showed conclusively that fructose was the dietary microangiopathic agent associated with sucrose-induced retinopathy. The microvascular lesions produced were similar to those found in diabetic rats maintained over the same period. Cross-sectional studies of the retinas revealed that microvascular lesions preceded the associated degeneration of neural tissue rather than vice versa since the majority of rats with retinopathy showed no signs of neural damage. Sucrose feeding was found to produce a significant elevation (p < 0.001) in blood fructose concentration and a slight increase, albeit not significant (p < 0.01), in retinal fructose-1-phosphate (F1P) levels. The results are discussed in relation to the changes in retinal sorbitol, fructose, FIP, and lactate metabolism found in diabetes.
为了确定蔗糖中的果糖部分还是微血管系统完整性所必需的某些因素的缺乏导致了大鼠蔗糖性视网膜病变的发生，在6个月的时间里对一系列含有这种因素和/或果糖可能来源的饮食进行了测试。对分离出的大鼠视网膜血管系统的检查确凿地表明，果糖是与蔗糖诱导的视网膜病变相关的饮食性微血管病变因子。所产生的微血管病变与同期维持的糖尿病大鼠中发现的病变相似。对视网膜的横断面研究表明，微血管病变先于相关的神经组织退化，而不是相反，因为大多数患有视网膜病变的大鼠没有神经损伤的迹象。发现喂食蔗糖会使血液中果糖浓度显著升高（p < 0.001），视网膜果糖-1-磷酸（F1P）水平略有升高，尽管不显著（p < 0.01）。结合糖尿病中发现的视网膜山梨醇、果糖、FIP和乳酸代谢的变化对结果进行了讨论。
