RETINOPATHY IN GALACTOSEMIC DOGS CONTINUES TO PROGRESS AFTER CESSATION OF GALACTOSEMIA
RETINOPATHY IN GALACTOSEMIC DOGS CONTINUES TO PROGRESS AFTER CESSATION OF GALACTOSEMIA
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DOI：
10.1001/archopht.1995.01100030111032
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发表时间：
1995-03-01
影响因子：
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通讯作者：
KERN, TS
中科院分区：
文献类型：
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作者：
ENGERMAN, RL;KERN, TS
背景：在人类和动物模型中，糖尿病视网膜病变的进展很难通过强化胰岛素治疗和严格的血糖控制及时停止。目的：为了了解这种抗停搏是否是糖尿病和胰岛素治疗所特有的，还是高血糖本身的特征，我们在半乳糖喂养的非糖尿病动物模型中确定了干预对糖尿病样视网膜病变的影响。方法：给狗喂食30%半乳糖的饲粮，24个月后分为两组，一组继续喂食半乳糖，另一组立即开始喂食不含半乳糖的饲粮。所有的动物在60个月的研究后被杀死。结果：正如预期的那样，食用富含半乳糖的饮食导致了半乳糖血症，表现为血红蛋白Ai、血浆非酶糖化蛋白和红细胞多元醇浓度升高，在停止食用半乳糖后，这些指标均降至正常水平。在半乳糖饮食24个月结束时，视网膜病变被发现是模棱两可的，尽管停止了半乳糖饮食，但随后进展明显。结论：视网膜病变在干预后没有立即停止的事实与先前糖尿病犬的数据一致，这表明血管病变可能是由于过量组织醛己糖的后遗症，而没有通过纠正醛己糖水平来及时纠正。
Background: Progression of diabetic retinopathy in human subjects and animal models is difficult to halt promptly by intensified insulin therapy and strict glycemic control.Objective: To learn whether this resistance to arrest is peculiar to diabetes and insulin therapy or is a characteristic of hyperglycemia itself, we have determined the effect of intervention on diabetic-like retinopathy in a nondiabetic animal model, the galactose-fed dog.Methods: Dogs were given a 30% galactose diet, At the end of 24 months, the dogs were divided into two groups, one of which continued to receive the galactose diet, while the second immediately began receiving the diet minus galactose. All animals were killed after 60 months of study.Results: Consumption of the galactose-rich diet resulted, as expected, in galactosemia evident by elevated hemoglobin Ai, plasma nonenzymatically glycated protein, and erythrocyte polyol concentrations, each of which decreased to normal levels following withdrawal of dietary galactose. Retinopathy was found to be equivocal at the end of 24 months of the galactose diet and subsequently progressed significantly despite cessation of the galactose diet.Conclusion: The fact that retinopathy did not halt promptly at intervention is consistent with previous data from diabetic dogs and suggests that the vascular lesions may be due to sequelae of excessive tissue aldohexose that are not promptly corrected by correction of the aldohexose level.