Abstract：
High sugar-sweetened beverage intake has been related to human kidney disease and metabolic alterations. We determine the impact of high sucrose intake from pregnancy until early postnatal days and post-weaning on kidneys from adult male offspring rats. Wistar female rats were mated and assigned into two groups: one control drinking tap water (CM) and another drinking 5 % sucrose diluted in water (SM). Two offspring per mother were randomly allocated into two experimental groups at weaning. One had free access to simple water (CO) and the other to 5 % sucrose (SO) for 14 weeks. After treatment, levels of relative aquaporin-2 (AQP2), glomerulosclerosis index (GI), collecting tube area, perirenal fat, blood creatinine, and blood ureic nitrogen concentration (BUN) were determined. Two-way ANOVA followed by Bonferroni post-hoc test was used, considering P ≤ 0.05 as a significant statistical difference. Sucrose consumption during gestation/lactation and interaction increased AQP2 expression in the renal cortex and BUN concentration. In contrast, gestation/lactation consumption increased collecting tube area, post-weaning consumption favored perirenal fat, and finally, gestation/lactation, post-weaning, and the interaction caused glomerulosclerosis. Our results suggest that the consumption of sucrose water during gestation/lactation or post-weaning or combination triggers pathological changes in the kidneys of adult rats.
摘要：
高糖饮料的摄入与人类的肾脏疾病和代谢改变有关。我们确定从怀孕到出生早期的高蔗糖摄入量的影响，在成年雄性后代大鼠的肾脏断奶后。将Wistar雌性大鼠交配并分成两组:一组对照饮用自来水(CM),另一组饮用在水中稀释的5%蔗糖(SM)。断奶时,每个母亲两个后代被随机分配到两个实验组，其中一个可以自由使用简单的水（CO），另一个可以自由使用5％的蔗糖（SO），持续14周。治疗后,相对水通道蛋白2（AQP2）水平，肾小球硬化指数（GI），收集管面积,肾周脂肪,测定肌酐和血尿素氮浓度（BUN）。考虑到P≤0.05是显着的统计学差异，使用了双向方差分析和Bonferronipost-hoc检验。妊娠/哺乳期间的蔗糖消耗和相互作用显示肾皮质中AQP2表达和BUN浓度增加，而妊娠/哺乳期消耗增加了收集管面积，断奶后消耗肾周脂肪增加，最后，妊娠/哺乳期，断奶后和相互作用导致肾小球硬化。我们的结果表明，在妊娠/哺乳期或断奶后或组合期间食用蔗糖水会引发成年大鼠肾脏的病理变化。
