Rizkalla S W, Boillot J, Tricottet V, Fontvieille A M, Luo J, Salzman J L, Camilleri J P, Slama G
Department of Diabetes (Inserm U341), Hotel Dieu Hospital, Paris, France.
Br J Nutr. 1993 Jul;70(1):199-209. doi: 10.1079/bjn19930117.
Sucrose feeding over a long period has been reported to induce glomerular basement membrane (GBM) thickening and insulin resistance in normal rats. These effects are attributed to the fructose moiety of the sucrose molecule, to Cu deprivation or both. Consequently, our aim was to evaluate the long-term effects of fructose feeding with normal or high amounts of Cu on body weight, plasma lipids, blood glucose regulation, GBM thickening and insulin binding to adipocytes. Four groups of eight Sprague-Dawley rats were fed for 10 weeks on a diet containing 570 g carbohydrate/kg supplied either as starch (S), dextrose (D), fructose (F) or fructose-starch (1:1, w/w; FS), and an adequate amount of Cu (12 micrograms Cu/g diet). A fifth group was fed on diet F supplemented with 24 micrograms Cu/g diet (FCu). After 10 weeks the epididymal adipose tissue and kidney weights expressed per 100 g body weight (relative weight) were heaviest in the F and FCu groups (P < 0.0001, ANOVA). The GBM thickness was within the normal range in the five groups but significantly higher in group D (1.95 (SE 0.04) nm and lower in group FS (1.79 (SE 0.02) nm when compared with group S (1.85 (SE 0.03) nm; P < 0.05). Insulin binding to adipocytes (expressed per cell) was lowest in the F and FCu groups, intermediate in groups D and FS and highest in group S (P < 0.05). Fasting plasma insulin level was higher in group F than in the FCu and FS groups (P < 0.05), whereas fasting plasma glucose, total cholesterol and triacylglycerol levels remained within the normal range in all groups. We conclude that in normal rats a 10-week fructose-rich diet with an adequate amount of Cu produced deleterious metabolic effects on adipose tissue, insulin binding to adipocytes, and plasma insulin, but not on GBM thickening even though kidney weight was significantly increased. However, a moderate fructose intake mixed with other sugars did not have adverse effects.
据报道，长期喂食蔗糖会导致正常大鼠的肾小球基底膜（GBM）增厚和胰岛素抵抗。这些影响归因于蔗糖分子的果糖部分、铜缺乏或两者兼有。因此，我们的目的是评估正常或高铜量饮食下长期喂食果糖对体重、血脂、血糖调节、GBM增厚以及胰岛素与脂肪细胞结合的影响。将四组每组八只Sprague-Dawley大鼠喂食含570 g碳水化合物/kg的饮食10周，碳水化合物分别以淀粉（S）、葡萄糖（D）、果糖（F）或果糖-淀粉（1:1，w/w；FS）形式提供，并含有适量的铜（12微克铜/克饮食）。第五组喂食补充有24微克铜/克饮食的F饮食（FCu）。10周后，F组和FCu组每100克体重的附睾脂肪组织和肾脏重量（相对重量）最重（P < 0.0001，方差分析）。五组的GBM厚度均在正常范围内，但与S组（1.85（标准误0.03）nm）相比，D组显著更高（1.95（标准误0.04）nm），FS组更低（1.79（标准误0.02）nm；P < 0.05）。胰岛素与脂肪细胞的结合（以每个细胞表示）在F组和FCu组中最低，在D组和FS组中居中，在S组中最高（P < 0.05）。F组的空腹血浆胰岛素水平高于FCu组和FS组（P < 0.05），而所有组的空腹血浆葡萄糖、总胆固醇和三酰甘油水平均保持在正常范围内。我们得出结论，在正常大鼠中，含适量铜的10周高果糖饮食对脂肪组织、胰岛素与脂肪细胞的结合以及血浆胰岛素产生了有害的代谢影响，但对GBM增厚没有影响，尽管肾脏重量显著增加。然而，适度摄入果糖与其他糖类混合并没有不良影响。
