Mohanam S, Bose S M
Acta Diabetol Lat. 1984 Jul-Sep;21(3):203-10. doi: 10.1007/BF02642893.
GAG metabolism was investigated in rats with experimentally induced diabetes. In comparison to control animals, the uptake of 35S-sulfate was diminished in tissues of diabetic animals. Streptozotocin-induced diabetes showed a significant decrease in the content of GAG fractions except that of non-sulfated GAG in liver and kidney which was unchanged as compared to the control group. In rats rendered diabetic by alloxan, non-sulfated GAG increased appreciably in liver and kidney whereas highly sulfated GAG remained unchanged. In the skins of alloxan-diabetic rats both total and sulfated GAG decreased significantly. The activities of liver beta-glucuronidase, beta-N-acetyl glucosaminidase and cathepsin D were significantly increased in rats treated with streptozotocin and alloxan. In streptozotocin-diabetic rats, renal beta-glucuronidase and beta-N-acetyl glucosaminidase activities were reduced while cathepsin D activity was similar to that of controls. The renal beta-N-acetyl glucosaminidase and cathepsin D activities of alloxan-treated rats were not significantly different from normal but their beta-glucuronidase was significantly increased. In the spleen of streptozotocin-diabetic rats all the enzymes were increased except beta-N-acetyl glucosaminidase which remained unaltered. Increased excretion of uronic acid was observed in diabetic groups. These results collectively indicate that both streptozotocin- and alloxan-induced diabetes altered the synthesis and catabolism of GAG.
在实验性诱导糖尿病的大鼠中研究了糖胺聚糖(GAG)代谢。与对照动物相比,糖尿病动物组织中35S-硫酸盐的摄取减少。链脲佐菌素诱导的糖尿病显示,除肝脏和肾脏中未硫酸化的GAG含量与对照组相比未改变外,GAG各组分的含量显著降低。在四氧嘧啶诱导糖尿病的大鼠中,肝脏和肾脏中未硫酸化的GAG明显增加,而高度硫酸化的GAG保持不变。在四氧嘧啶糖尿病大鼠的皮肤中,总GAG和硫酸化GAG均显著降低。用链脲佐菌素和四氧嘧啶处理的大鼠肝脏β-葡萄糖醛酸酶、β-N-乙酰氨基葡萄糖苷酶和组织蛋白酶D的活性显著增加。在链脲佐菌素糖尿病大鼠中,肾脏β-葡萄糖醛酸酶和β-N-乙酰氨基葡萄糖苷酶活性降低,而组织蛋白酶D活性与对照组相似。四氧嘧啶处理大鼠的肾脏β-N-乙酰氨基葡萄糖苷酶和组织蛋白酶D活性与正常组无显著差异,但它们的β-葡萄糖醛酸酶显著增加。在链脲佐菌素糖尿病大鼠的脾脏中,除β-N-乙酰氨基葡萄糖苷酶保持不变外,所有酶均增加。糖尿病组观察到糖醛酸排泄增加。这些结果共同表明,链脲佐菌素和四氧嘧啶诱导的糖尿病均改变了GAG的合成和分解代谢。