Sugiyama S, Miyata T, Ueda Y, Tanaka H, Maeda K, Kawashima S, Van Ypersele de Strihou C, Kurokawa K
Chukyo Hospital, Nagoya, Japan.
J Am Soc Nephrol. 1998 Sep;9(9):1681-8. doi: 10.1681/ASN.V991681.
Nonenzymatic reactions between glucose and proteins yield advanced glycation end products (AGE) such as pentosidine. AGE accumulate in diabetic patients, alter the structure and function of tissue proteins, stimulate cellular response, and have thus been implicated in diabetic tissue damage. The present study was undertaken to assess the factors determining plasma total pentosidine level in diabetic patients and the possible relation between plasma pentosidine level and diabetic complications. In diabetic patients, including patients with renal failure, plasma pentosidine levels, assessed by HPLC assay, were correlated with serum creatinine (P < 0.0001). In patients with normal renal function, pentosidine levels were correlated with blood glucose control (hemoglobin Alc: P = 0.0028; fructoselysine: P = 0.0133), serum creatinine (P = 0.029), patient age (P = 0.0416), duration of diabetes (P = 0.0431), and total cholesterol (P = 0.0056) and LDL-cholesterol (P = 0.0208). Multiple regression analysis revealed an independent influence of hemoglobin Alc and serum creatinine on pentosidine levels (r2 = 0.216, P = 0.0026). Pentosidine levels were higher in patients with than in those without hypertension (P = 0.043) or ischemic heart diseases (P = 0.0061). No such differences were observed between patients with and without albuminuria or retinopathy. Multiple regression analysis revealed an independent influence of plasma pentosidine on the presence of hypertension (r2 = 0.129, P = 0.0382) and of plasma pentosidine and HDL-cholesterol on the presence of ischemic heart disease (r2 = 0.326, P = 0.0012). The present study demonstrated that plasma pentosidine level was significantly influenced by the quality of glycemic control and renal function. Pentosidine level was also correlated with hypertension and ischemic heart disease, and might be taken as a biomarker of diabetic cardiovascular risk.
葡萄糖与蛋白质之间的非酶促反应会产生诸如戊糖苷等晚期糖基化终产物（AGE）。AGE在糖尿病患者体内蓄积，会改变组织蛋白的结构和功能，刺激细胞反应，因此被认为与糖尿病组织损伤有关。本研究旨在评估决定糖尿病患者血浆总戊糖苷水平的因素，以及血浆戊糖苷水平与糖尿病并发症之间的可能关系。在糖尿病患者中，包括肾衰竭患者，通过高效液相色谱法测定的血浆戊糖苷水平与血清肌酐相关（P < 0.0001）。在肾功能正常的患者中，戊糖苷水平与血糖控制（糖化血红蛋白：P = 0.0028；果糖赖氨酸：P = 0.0133）、血清肌酐（P = 0.029）、患者年龄（P = 0.0416）、糖尿病病程（P = 0.0431）、总胆固醇（P = 0.0056）和低密度脂蛋白胆固醇（P = 0.0208）相关。多元回归分析显示糖化血红蛋白和血清肌酐对戊糖苷水平有独立影响（r2 = 0.216，P = 0.0026）。有高血压患者的戊糖苷水平高于无高血压患者（P = 0.043），有缺血性心脏病患者的戊糖苷水平高于无缺血性心脏病患者（P = 0.0061）。在有蛋白尿或视网膜病变的患者与无蛋白尿或视网膜病变的患者之间未观察到此类差异。多元回归分析显示血浆戊糖苷对高血压的存在有独立影响（r2 = 0.129，P = 0.0382），血浆戊糖苷和高密度脂蛋白胆固醇对缺血性心脏病的存在有独立影响（r2 = 0.326，P = 0.0012）。本研究表明血浆戊糖苷水平受血糖控制质量和肾功能的显著影响。戊糖苷水平还与高血压和缺血性心脏病相关，可能可作为糖尿病心血管风险的生物标志物。
