McLennan S, Yue D K, Fisher E, Capogreco C, Heffernan S, Ross G R, Turtle J R
Department of Medicine, University of Sydney, NSW, Australia.
Diabetes. 1988 Mar;37(3):359-61. doi: 10.2337/diab.37.3.359.
The plasma and tissue concentration of ascorbic acid (AA) is reduced in diabetes. This study was designed to investigate the mechanism and significance of this phenomenon. The low plasma AA concentration of diabetic rats can be normalized by dietary AA supplement (20-40 mg/day), a dosage approximately equal to the maximal synthetic rate of this substance in the rats. Treatment of diabetic rats with this regime prevented the decrease in activity of granulation tissue prolyl hydroxylase (PRLase), an AA-dependent enzyme required for maintaining the normal properties of collagen. The decreased plasma AA concentration and granulation tissue PRLase activity in diabetes can also be normalized by the aldose reductase inhibitor tolrestat. We conclude that in diabetic animals there is a true deficiency of AA that may be responsible for some of the changes of collagen observed in diabetes. Treatment with AA or an aldose reductase inhibitor may prevent some of the diabetic complications with underlying collagen abnormalities.
糖尿病患者体内抗坏血酸（AA）的血浆和组织浓度会降低。本研究旨在探究这一现象的机制及意义。通过饮食补充AA（20 - 40毫克/天）可使糖尿病大鼠的低血浆AA浓度恢复正常，该剂量大致等同于大鼠体内该物质的最大合成速率。用此方案治疗糖尿病大鼠可防止肉芽组织脯氨酰羟化酶（PRLase）活性降低，PRLase是一种维持胶原蛋白正常特性所需的AA依赖酶。糖尿病患者血浆AA浓度降低及肉芽组织PRLase活性降低也可通过醛糖还原酶抑制剂托瑞司他恢复正常。我们得出结论，在糖尿病动物中存在真正的AA缺乏，这可能是糖尿病中观察到的一些胶原蛋白变化的原因。用AA或醛糖还原酶抑制剂治疗可能预防一些存在潜在胶原蛋白异常的糖尿病并发症。
