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作 者:杨春[1] 严棠 陈玉驹[1] 傅祖植[1] 钟光恕[1] 程桦[1]
机构地区:[1]中山医科大学孙逸仙纪念医院内科
出 处:《中华内分泌代谢杂志》1991年第1期20-23,共4页Chinese Journal of Endocrinology and Metabolism
基 金:国家教育委员会科学基金资助项目
摘 要:采用乳过氧化物酶法制备A_(14)-^(125)I胰岛素,泛影葡胺-聚蔗糖分层液密度梯度离心法分离外周血单个核细胞,优选受体结合试验条件,建立了单个核细胞胰岛素受体放射分析法。测定了54例NIDDM患者、29例单纯肥胖症患者和27例正常人的单个核细胞胰岛素受体结合率(MIB)。结果表明NIDDM组的MIB显著低于正常组,空腹血浆胰岛素(FPI)高于正常组;NIDDM肥胖型组中MIB与FPI呈负相关。证实胰岛素受体缺陷是NIDDM产生胰岛素抵抗性的重要原因之一。Monocyte insulin binding (MIB) was detei mined by receptor-radioassay in 54 NIDDM patients (obese 32, non- obese 22) and 56 non-diabetic subjects (obese 29, normal control 27). The experimental conditions were optimized. A fixed amount of labelled and urt-labelled insulin was selected for an one-point assay of MIB. Fasting plasma insulin (FPI) levels were higher in NIDDM patients and obese non-diabetics than in normal controls. MIB was significantly lower in the obese than in the normal control (1.82±0.18% vs 2.94±0.70%, P<0.002). MIB in both obese and nonobese NIDDM patients (1.58±0.14%, 1.76±0.18 % respectively) were also significantly lower (P<0.001) than that in the normal controls, but the difference was not significant when compared with the results in the obese nondiabetic eroup. A negative correlation was observed between MIB and FPI in obese diabetics, This decrease of MIB in obese diabetics could be explained, at least in part,by the mechanism of down regulation, but the decrease in non-obese diabetics could hardly be explained by the same mechanism because no close correlation was demonstrated between MIB and FPI in these patients. It suggested that obesity and/or hyperinsulin were not the only factors for the insulin resistance in diabetics.
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