摘要
目的 :探讨原发性肾病综合征患者是否存在胰岛素抵抗以及其发生机理和肾组织ISNR β、CPR、eNOS的表达。 方法 :检测 46例原发性肾病综合征患者和 2 0例健康对照者空腹血清葡萄糖 (FG)、空腹血清胰岛素 (FISN)和空腹血清C 肽 (FCP)水平 ,计算胰岛素敏感指数 (ISI)。分析ISI与血压、血脂、肾功能变化的关系。应用免疫组织化学法检测肾组织胰岛素受体 β(ISNR β)、C 肽受体 (CPR)和内皮型一氧化氮合成酶 (eNOS)的表达。 结果 :原发性肾病综合征患者FG、FISN、FCP的水平显著高于对照组 ,ISI显著低于对照组 ,且患者ISI的降低与甘油三酯、低密度脂蛋白、血尿酸的升高呈显著负相关。患者肾组织IS NR β、CPR和eNOS的表达较对照肾组织无显著改变。 结论 :原发性肾病综合征患者存在血糖、胰岛素和C 肽水平的升高及胰岛素抵抗。其原因可能与血压升高、血脂和尿酸代谢紊乱等有关。患者肾组织ISNR β、CPR和eNOS的表达无显著变化。
Objective To investigate insulin resistance (IR),its existent and its possible pathogenesis, the expression of insulin receptor beta(INSR、β),C、peptide receptor(CPR) and endothelial nitric oxide synthase(eNOS)in renal tissue in primary nephrotic syndrome patients.Methods Of all the patients and normal controls,fasting serum glucose(FG), insulin(FISN), C、peptide(FCP) were detected, insulin sensitive index(ISI) was calculated by the formula previously reported.The reported before. The relationship between ISI and blood lipid, ISI and renal function, were investigated. The expression of ISNR、β,CPR and eNOS in renal organism were detected by immunohistochemical staining technique. Results Compared with normal controls, the concentration of FG, FISN, FCP increased significantly(P<0.01 or P<0.05), and ISI decreased significantly(P<0.01)in primary nephrotic syndrome patients.Their ISI correlated negatively with triglyceride(TG) (P< 0.05),low density lipoprotein cholesterol(LDL、c)(P<0.05) and blood uric acid(UA)(P<0.01). While,the expressions of INSR、β,CPR and eNOS in renal organism had no statistical differences between patients and controls. Conclusion Primary nephrotic syndrome patients have insulin resistance and increased concentrations of blood glucose, insulin and C、peptide,the possible reasons for which are blood pressure rise, derangement of blood lipid and UA. While the expression of ISNR、β,CPR and eNOS in renal organism has no significant change in primary nephrotic syndrome patients.
出处
《东南大学学报(医学版)》
CAS
2004年第5期298-303,共6页
Journal of Southeast University(Medical Science Edition)