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139例原发性痛风患者胰岛β细胞功能的分析 被引量:1

Analysis of the function of islet β cell in 139 patients with primary gout
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摘要 目的探讨原发性痛风患者不同糖代谢状态胰岛β细胞功能的演变及高胰岛素血症(HIns)在其中的作用。方法纳入原发性痛风患者139例,分为正常血糖-非高胰岛素血症(A)组、正常血糖-高胰岛素血症(B)组、IGR(C)组及糖尿病(D)组。统计及测量相关指标,计算IR相关指标。结果(1)A、C、D、B组胰岛素抵抗指数(HOMA-IR)依次升高,而ISI水平依次降低。除A组与C组外,其他组间HOMA-IR及ISI比较差异有统计学意义(P<0.05)。B组HOMA-IR及早时相胰岛素分泌指数(ΔI30/ΔG30)高于A组,而ISI低于A组(P<0.05);B组胰岛β细胞功能指数(HOMA-β)高于D组(P<0.05)。(2)回归分析显示,FIns、Ins 120min、HOMA-β、HOMA-IR、ΔI30/ΔG30与糖尿病独立相关,SUA水平与糖尿病无关。结论 IR、胰岛β细胞分泌障碍及胰岛素水平升高是原发性痛风患者发展为糖尿病的主要代谢特征。早期预防糖尿病应更加关注出现HIns但血糖正常的人群。 Objective To explore the function of islet β cell and hyperinsulinemia in patients with primary gout at different status of glucose metabolism.Methods A total of 139 patients with primary gout were divided into normal glucose tolerance-non-hyperinsulinemia (A) group,normal glucose tolerance-hyperinsulinemia (B) group,impaired glucose regulation (C) group,and diabetes mellitus (D) group.Correlation indexes were measured,and the related indexes of insulin resisitance were calculated.Results (1) The levels of HOMA-1R were progressively increased from A to C to D to B groups,while the levels of ISI were progressively decreased.The differences of HOMA-IR and ISI were statistically significant among groups except group A and group C(P<0.05).The levels of HOMA-IR,△I30/G30were significantly higher in group B than in group A,while ISI was significantly lower(P<0.05).The levels of HOMA-β were significantly higher in group B than in group D (P<0.05).(2)The binary logistic regression indicated that FIns,Ins 120 min,HOMA-β,HOMA-IR,△I30/△G30 were independently associated with diabetes,but not the SUA.Conclusion Insulin resistance,islet β cell dysfunction,and increased insulin level may be the main metabolic features in gout patients with diabetes.Consequently,more attention should be paid to the screening of population with hyperinsulinemic-NGT.
出处 《中国糖尿病杂志》 CAS CSCD 北大核心 2014年第6期485-487,共3页 Chinese Journal of Diabetes
关键词 痛风 原发性 胰岛Β细胞功能 高胰岛素血症 糖代谢 胰岛素抵抗 Gout,primary Islet β cell function Hyperinsulinemia Glucose metabolism Insulin resistance
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