Dunger A, Berg S, Klöting I, Schmidt S
Institute of Diabetes Gerhardt Katsch Karlsburg, Germany.
Exp Clin Endocrinol Diabetes. 1997;105 Suppl 2:48-50. doi: 10.1055/s-0029-1211797.
The aim of this study was to compare the effect of long-term diabetes with that of a long-term high protein diet in vivo on the kidney function and in vitro on cellular parameters of isolated glomeruli of BB rats. Four groups of rats were investigated: Group 1 = normoglycaemic (N) rats > 250 days old; group 2 = age-matched diabetic (D) rats with a diabetes duration of more than 150 days; group 3 = BB rats which were fed a protein diet of 8% (low protein = LP) and group 4 = rats which received a high protein (HP) diet (32%) for more than 80 weeks. From 24-h-urine samples albumin, urea, creatinine and electrolyte excretion were estimated. At the end of the study the total kidney weight was determined and glomeruli were isolated for in vitro experiments. Hyperglycaemic and HP fed rats were characterised by a significantly increased excretion of albumin, urea and different electrolytes compared to normoglycaemic or LP fed animals. Creatinine excretion was neither affected by hyperglycaemia nor HP diet. HP and D caused a significant increase in total kidney weight when compared to the LP and N group, respectively (N: 1.79 +/- 0.08; D: 2.33 +/- 0.09; LP: 2.26 +/- 0.18; HP: 3.28 +/- 0.46 g; p < 0.05). The increased kidney weight of diabetic and HP rats correlated well with a significant enhanced DNA content of isolated glomeruli (N: 3.41 +/- 0.15; D: 4.45 +/- 0.19; LP: 4.18 +/- 0.35; HP: 6.40 +/- 0.62 micrograms/1000 glomeruli; p < 0.02). In addition, glomeruli obtained from either D or HP fed BB rats incorporated significantly more 3H-thymidine into their DNA indicating an elevated rate of DNA synthesis. The results demonstrate that HP diet caused markedly altered kidney function and induced cellular changes of glomeruli which are interpreted as enhanced proliferative processes. These alterations are comparable to those associated with diabetes mellitus. An unbalanced high protein diet represents a considerable risk factor for the development of functional and structural impairments of the kidney and should absolutely be avoided in patients suffering from diseases which are known to be associated with kidney alterations.
本研究的目的是比较长期糖尿病与长期高蛋白饮食在体内对肾功能的影响,以及在体外对BB大鼠分离肾小球细胞参数的影响。研究了四组大鼠:第1组=血糖正常(N)且年龄大于250天的大鼠;第2组=年龄匹配、糖尿病病程超过150天的糖尿病(D)大鼠;第3组=喂食8%蛋白质饮食(低蛋白=LP)的BB大鼠;第4组=接受高蛋白(HP)饮食(32%)超过80周的大鼠。从24小时尿液样本中估算白蛋白、尿素、肌酐和电解质排泄量。在研究结束时,测定肾脏总重量,并分离肾小球用于体外实验。与血糖正常或喂食LP的动物相比,高血糖和喂食HP的大鼠白蛋白、尿素和不同电解质的排泄量显著增加。肌酐排泄量既不受高血糖影响,也不受HP饮食影响。与LP组和N组相比,HP组和D组分别导致肾脏总重量显著增加(N组:1.79±0.08;D组:2.33±0.09;LP组:2.26±0.18;HP组:3.28±0.46 g;p<0.05)。糖尿病和HP大鼠肾脏重量增加与分离肾小球DNA含量显著增加密切相关(N组:3.41±0.15;D组:4.45±0.19;LP组:4.18±0.35;HP组:6.40±0.62微克/1000个肾小球;p<0.02)。此外,从喂食D或HP的BB大鼠获得的肾小球将显著更多的3H-胸腺嘧啶核苷掺入其DNA中,表明DNA合成速率升高。结果表明,HP饮食导致肾功能明显改变,并诱导肾小球细胞变化,这被解释为增殖过程增强。这些改变与糖尿病相关的改变相当。不均衡的高蛋白饮食是肾脏功能和结构损害发展的一个相当大的危险因素,对于已知与肾脏改变相关疾病的患者绝对应该避免。