Lockwood M K, Eckhert C D
School of Public Health, University of California, Los Angeles 90024-1772.
Am J Physiol. 1992 Jan;262(1 Pt 2):R144-9. doi: 10.1152/ajpregu.1992.262.1.R144.
Injury to microvessels caused by the chronic consumption of sucrose can be prevented by selenium (Se). The objective of this study was to determine the temporal sequence of changes in serum triglycerides, total cholesterol, glucose, and insulin induced by sucrose and their relationship to Se status and microvascular injury. Two groups of 24 Wistar rats were fed ad libitum diets in which the entire carbohydrate was either corn starch or sucrose. Two other groups were fed identical diets supplemented with 0.1 micrograms Se/g. At 6, 8, and 10 mo, eight rats from each group were fasted for 12 h and had blood taken. Rats were then given a glucose tolerance test and killed, and their retinal microvessels were evaluated for injury. After 6 mo, sucrose-fed rats had elevated triglycerides and total cholesterol. Abnormal glucose clearance and hyperinsulemia developed after 8 mo. Evidence of microvascular injury became apparent after 10 mo. These changes did not occur in rats provided the starch-based diets, and microvascular injury did not develop in the sucrose-fed rats provided supplemental Se. Glutathione peroxidase activity was normal in all groups throughout the 10-mo experiment. These results chronicle the sucrose-induced systemic insult and show that the protective effect of Se does not occur by diminishing this insult to the microvessels.
长期食用蔗糖导致的微血管损伤可被硒（Se）预防。本研究的目的是确定蔗糖诱导的血清甘油三酯、总胆固醇、葡萄糖和胰岛素变化的时间顺序，以及它们与硒状态和微血管损伤的关系。两组24只Wistar大鼠随意进食，其全部碳水化合物分别为玉米淀粉或蔗糖。另外两组喂食添加了0.1微克硒/克的相同饮食。在6、8和10个月时，每组8只大鼠禁食12小时后采血。然后给大鼠进行葡萄糖耐量试验并处死，评估其视网膜微血管损伤情况。6个月后，喂食蔗糖的大鼠甘油三酯和总胆固醇升高。8个月后出现葡萄糖清除异常和高胰岛素血症。10个月后微血管损伤的证据变得明显。这些变化在喂食淀粉类饮食的大鼠中未出现，在喂食蔗糖的大鼠中补充硒后也未发生微血管损伤。在整个10个月的实验中，所有组的谷胱甘肽过氧化物酶活性均正常。这些结果记录了蔗糖诱导的全身损伤，并表明硒的保护作用不是通过减轻对微血管的这种损伤来实现的。
