CAJ | 학술논문

目的探讨糖尿病状态下肾小球蛋白激酶C(PKC)与肾脏改变的关系。方法对链脲菌素诱发的糖尿病大鼠喂养28周，同时对部分糖尿病大鼠进行胰岛素治疗。测定糖尿病大鼠血糖、糖化血红蛋白A1c(HbA1c)、PKC活性、肾小球基底膜厚度（GBMT）和尿蛋白质/肌酐（Pr/Cr）比值，并与正常对照组比较。结果糖尿病大鼠在血糖水平和HbA1c含量增高的同时，PKC活性、GBMT和尿Pr/Cr比值都显著增加(P<0.01)；PKC活性与血糖相关（P<0.01),而与HbA1c无显著相关性(P>0.05)，胰岛素治疗可通过降低血糖水平来减少HbA1c形成、改善PKC活性，从而减缓GBMT增加，减少尿蛋白排出。结论高血糖慢性刺激可引起肾小球PKC活性增高，非酶促糖基化可能未直接参与PKC活性改变，PKC活性长期增高可促进糖尿病肾病发生与发展。
목적 탐토당뇨병상태하신소구단백격매C(PKC)여신장개변적관계。방법 대련뇨균소유발적당뇨병대서위양28주，동시대부분당뇨병대서진행이도소치료。측정당뇨병대서혈당、당화혈홍단백A1c(HbA1c)、PKC활성、신소구기저막후도（GBMT）화뇨단백질/기항（Pr/Cr）비치，병여정상대조조비교。결과 당뇨병대서재혈당수평화HbA1c함량증고적동시，PKC활성、GBMT화뇨Pr/Cr비치도현저증가(P<0.01)；PKC활성여혈당상관（P<0.01),이여HbA1c무현저상관성(P>0.05)，이도소치료가통과강저혈당수평래감소HbA1c형성、개선PKC활성，종이감완GBMT증가，감소뇨단백배출。결론 고혈당만성자격가인기신소구PKC활성증고，비매촉당기화가능미직접삼여PKC활성개변，PKC활성장기증고가촉진당뇨병신병발생여발전。
Objective To evaluate the relationship between glomerular proteinkinase C (PKC) and renal alterations under diabetic state. Methods The streptozotocin-induced diabetic rats were fed for 28 weeks. Insulin was administered to some of them after the onset of diabetes. Then blood glucose, hemoglobin Alc (HbAlc), glomerular PKC activity, glomerular basement membrane thickness (GBMT) and urine protein/creatinine (Pr/Cr) ratio in diabetic rats were measured and compared with those in the control. Results The levels of blood glucose, HbAlc content, PKC activity and GBMT were significantly higher in diabetic rats than those in the control (P<0.01). Insulin treatment could decrease the levels of blood glucose, reduce HbAlc content, ameliorate PKC activity and delay the thickening of glomerular basement membrance (GBM). Conclusion Chronic stimulation of hyperglycemia may increase PKC activity. Nonenzymatic glycosylation may not directly contribute to increasing PKC activity. Long-term increase of PKC activity may enhance the development and progression of diabetic nephropathy.