Saari J T, Bode A M, Dahlen G M
U.S. Department of Agriculture, Agricultural Research Service, Grand Forks Human Nutrition Research Center, ND, USA.
J Nutr. 1995 Dec;125(12):2925-34. doi: 10.1093/jn/125.12.2925.
We examined the hypothesis that nonenzymatic glycosylatin of proteins (glycation) contributes to the defects of copper deficiency. We studied copper-adequate and -deficient rats while altering two factors known to affect glycation: type of dietary carbohydrate and amount of food intake. Copper deficiency caused cardiac enlargement and anemia, decreased erythrocyte osmotic fragility, enhanced heart lipid peroxidation, increased the percentage of glycated hemoglobin (Hb A1) and reduced staining of lens crystallins on SDS-PAGE gels (suggestive of glycation). Increasing dietary sucrose reduced organ copper concentration, exacerbated the rise in Hb A1 and worsened the anemia caused by copper deficiency. Food restriction ameliorated heart and erythrocyte defects, reduced the percentage of glycated hemoglobin and heart peroxidation and also improved heart and liver copper status in copper-deficient rats. These findings indicate that copper deficiency enhances glycation and that sucrose may exacerbate some defects of copper deficiency by enhancing glycation. Inhibition of defects of copper deficiency by food restriction suggests that glycation and/or peroxidation may contribute to those defects.
我们检验了蛋白质非酶糖基化（糖基化）导致铜缺乏缺陷的假说。我们研究了铜充足和铜缺乏的大鼠，同时改变已知会影响糖基化的两个因素：膳食碳水化合物类型和食物摄入量。铜缺乏导致心脏扩大和贫血，降低红细胞渗透脆性，增强心脏脂质过氧化，增加糖化血红蛋白（Hb A1）百分比，并减少SDS-PAGE凝胶上晶状体蛋白的染色（提示糖基化）。增加膳食蔗糖会降低器官铜浓度，加剧Hb A1的升高，并使铜缺乏引起的贫血恶化。食物限制改善了心脏和红细胞缺陷，降低了糖化血红蛋白百分比和心脏过氧化，并改善了铜缺乏大鼠的心脏和肝脏铜状态。这些发现表明，铜缺乏会增强糖基化，而蔗糖可能通过增强糖基化加剧铜缺乏的一些缺陷。食物限制对铜缺乏缺陷的抑制表明，糖基化和/或过氧化可能导致这些缺陷。
