Kalia Kiran, Sharma Seema, Mistry Kinnari
Department of Biosciences, Sardar Patel University, Vallabh Vidyanagar-388120 Gujarat, India.
Clin Chim Acta. 2004 Sep;347(1-2):169-76. doi: 10.1016/j.cccn.2004.04.016.
Diabetic nephropathy is a relatively common microvascular complication in people suffering from diabetic mellitus. Chronic hyperglycemia leads to the accumulation of advanced glycosylation end products (AGEs) that covalently trap extravasated serum proteins such as immunoglobulins, albumin, and LDL through glucose derived cross-linking to the extra vascular matrix.
Serum fructosamine, glycosylated hemoglobin and percent glycosylation of IgG, IgA, IgM were measured in five different groups of human subjects: 50 normal individuals; 40 type 2 DM patients; 42 type 1 DM patients; 40 type 2 DM patients with nephropathy and 37 type 1 DM patients with nephropathy.
Patients with long-term history of diabetes and chronic hyperglycemia as well as suffering from diabetic nephropathy showed an increased glycosylated hemoglobin level and serum fructosamine as compared to those with diabetes mellitus and to the normal individuals. Glycosylation of IgG, IgA and IgM showed an increase in both type 1 and type 2 DM patients with nephropathy as compared to the diabetic patients without any complication. A positive correlation has been observed between glycosylated IgG and glycosylated hemoglobin (R2=0.522, 0.5113, 0.7117, 0.673) in type 1 and type 2 DM without and with diabetic nephropathy, respectively, whereas correlation between glycosylated IgG and serum fructosamine was observed only in type 1 and type 2 DM without nephropathy (R2=0.7318, 0.5767).
The present study suggests that glycosylation of IgG is an equivalent marker for advanced glycosylation as GHb and may have some role to play in the on onset of diabetic nephropathy by altering their immunoreactivity leading to microvascular complications.
糖尿病肾病是糖尿病患者中较为常见的微血管并发症。慢性高血糖会导致晚期糖基化终产物(AGEs)的积累,这些产物通过葡萄糖衍生的交联作用与血管外基质共价结合,从而捕获诸如免疫球蛋白、白蛋白和低密度脂蛋白等渗出的血清蛋白。
在五组不同的人类受试者中测量血清果糖胺、糖化血红蛋白以及IgG、IgA、IgM的糖基化百分比:50名正常个体;40名2型糖尿病患者;42名1型糖尿病患者;40名患有肾病的2型糖尿病患者和37名患有肾病的1型糖尿病患者。
与糖尿病患者和正常个体相比,有长期糖尿病病史、慢性高血糖以及患有糖尿病肾病的患者糖化血红蛋白水平和血清果糖胺升高。与无任何并发症的糖尿病患者相比,1型和2型糖尿病肾病患者的IgG、IgA和IgM糖基化均增加。在无糖尿病肾病和有糖尿病肾病的1型和2型糖尿病中,分别观察到糖基化IgG与糖化血红蛋白之间存在正相关(R2 = 0.522、0.5113、0.7117、0.673),而仅在无肾病的1型和2型糖尿病中观察到糖基化IgG与血清果糖胺之间存在相关性(R2 = 0.7318、0.5767)。
本研究表明,IgG糖基化是与糖化血红蛋白相当的晚期糖基化标志物,可能通过改变其免疫反应性导致微血管并发症,从而在糖尿病肾病的发病中发挥一定作用。