DETECTION OF AUTOANTIBODIES AGAINST ISLET AMYLOID POLYPEPTIDE IN HUMAN SERUM - LACK OF ASSOCIATION WITH TYPE-1 (INSULIN-DEPENDENT) DIABETES-MELLITUS, OR WITH CONDITIONS FAVORING AMYLOID DEPOSITION IN ISLETS
DETECTION OF AUTOANTIBODIES AGAINST ISLET AMYLOID POLYPEPTIDE IN HUMAN SERUM - LACK OF ASSOCIATION WITH TYPE-1 (INSULIN-DEPENDENT) DIABETES-MELLITUS, OR WITH CONDITIONS FAVORING AMYLOID DEPOSITION IN ISLETS
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DOI：
10.1007/bf02221685
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发表时间：
1992-11-01
期刊：
影响因子：
8.2
通讯作者：
VANSCHRAVENDIJK, CFH
中科院分区：
文献类型：
--
作者：
GORUS, FK;SODOYEZ, JC;VANSCHRAVENDIJK, CFH
研究人员开发了一种检测胰岛淀粉样多肽自身抗体的放射结合试验，并对其进行了分析验证，并与检测胰岛素自身抗体的类似试验同时应用于新近发病的1型（胰岛素依赖）糖尿病患者和年龄和性别匹配的对照受试者的血清。胰岛淀粉样多肽自身抗体滴度在患者组和匹配的对照组之间没有差异，在受试者组内也没有根据年龄的差异。1型糖尿病发病时，30例0-19岁患者中仅有1例、35例20-39岁患者中仅有2例检测到胰岛淀粉样蛋白多肽-自身抗体水平升高（>为对照组的97百分位数）。相比之下，胰岛素自身抗体经常被发现，特别是在20岁以下的糖尿病患者中（0-19岁：30例患者中有18例；20-39岁：35例患者中有10例；与匹配的对照组相比p < 0.01）。3例胰岛素瘤患者和37例2型糖尿病患者（年龄33-70岁）均未检测到胰岛淀粉样多肽自身抗体（对照组40例中1例）。在阳性血清中，蛋白A-Sepharose吸附去除胰岛淀粉样多肽结合活性，从而证实其抗体性质。总之，1型糖尿病与年龄依赖性胰岛素自身抗体反应有关，但与胰岛淀粉样多肽无关。与胰岛淀粉样蛋白沉积相关的疾病（2型糖尿病、胰岛素瘤和衰老）不利于形成针对胰岛淀粉样蛋白多肽的自身抗体。
A radiobinding assay for the detection of autoantibodies against islet amyloid polypeptide was developed, analytically validated, and - in parallel with a similar assay for the detection of autoantibodies against insulin - applied to sera from recent-onset Type 1 (insulin-dependent) diabetic patients and from age- and sex-matched control subjects. There was no difference in islet amyloid polypeptide autoantibody titres between patient groups and matched control subjects, nor within subject groups according to age. At onset of Type 1 diabetes, elevated islet amyloid polypeptide-autoantibody levels (> 97th percentile of control subjects) were only detected in 1 of 30 patients aged 0-19 years and in 2 of 35 patients aged 20-39 years. By contrast, insulin autoantibodies were frequently demonstrated, in particular at onset of diabetes under age 20 (0-19 years: 18 of 30 patients; 20-39 years: 10 of 35 patients; p < 0.01 vs matched control subjects). Islet amyloid polypeptide autoantibodies were not detectable in 3 insulinoma patients nor ir 37 patients (aged 33-70 years) with Type 2 diabetes (vs 1 of 40 in matched control subjects). In positive serum, adsorption onto protein A-Sepharose removed islet amyloid polypeptide binding activity, hereby confirming its antibody nature. In conclusion, Type 1 diabetes is associated with an age-dependent autoantibody reaction against insulin but not against islet amyloid polypeptide. Conditions associated with amyloid deposition in islets (Type 2 diabetes, insulinoma and ageing) do not favour the formation of autoantibodies against islet amyloid polypeptide.