摘要
                
                    目的探讨不同糖耐量人群胰岛素抵抗(IR)和胰岛β细胞功能状态。方法分析5523例患者行OGTT和胰岛素释放试验的结果,根据WHO标准将研究对象分为糖代谢正常(NGT)组、单纯空腹血糖升高(IFG)组、单纯糖耐量减低(IGT)组、空腹血糖升高合并糖耐量受损(IFG+IGT)组和2型糖尿病(T2DM)组。结果(1)HOMA-IR:IFG、IGT、IFG+IGT和T2DM组比NGT组分别增加41%、19%、47%和69%(P<0.01)。(2)校正IR影响后,IFG、IGT、IFG+IGT和T2DM组比NGT组HOMA-β分别下降54%、19%、55%和68%,△I30/△G30分别下降47%、40%、63%和82%(P<0.001);IFG、IFG+IGT和T2DM组AUCI比NGT组分别下降27%、26%和30%(P<0.01)。结论(1)从IGT、IFG、IFG+IGT到T2DM发展过程中IR程度逐渐加重,胰岛β细胞早时相分泌和基础分泌功能逐渐衰竭,晚时相分泌代偿能力功能减弱,总体分泌功能逐渐减退。(2)从NGT、IGT、IFG、IFG+IGT到T2DM的糖代谢异常发生发展过程反映了胰岛β细胞早时相、基础和整体分泌功能逐渐衰退变化规律。
                
                Objective To clarify insulin resistances and pancreatic β-cell hypofunctions in cases with different glucose tolerance. Methods 5523 Chinese underwent OGTT and were classified into normal glucose tolerance (NGT), isolated impaired fasting glucose (IFG), isolated impaired glucose tolerance (IGT), IFG with IGT (IFG+IGT) and type 2 diabetes mellitus (T2DM) groups based on OGTT results. HOMA-IR, HOMA-β△I30/β△G30and AUCI of different groups were statistically analyzed by SPSS12.0.  Results ① Compared to NGT group, HOMA-IR was increased by 41%, 19 %, 47 % and 69 % respectively in IFG, IGT, IFG+IGT and T2DM groups (all P〈0. 001). ②Compared to NGT group after adjusted by HOMA-IR,the level of HOMA-β was decreased by 54%, 19%, 55% and 68% respectively in IFG, IGT, IFG+IGT and T2DM groups (all P〈0. 001);△I30/△G30 ratio was decreased by 47%, 40%, 63% and 82% (all P〈0. 001) ; AUCi was decreased by 27%, 26% and 30% respectively in IFG, FG+IGT and T2DM groups (all P〈0. 001). Conclusions ①From NGT, IGT,IFG, IFG+IGT to T2DM, insulin resistance was getting heavier;The compensation of insulin secretion after glucose load and insulin secretions at baseline,early stage and total were decreased progressively. ②Developing history of T2DM can reflect character of islet β-cell dysfunction.
    
    
    
    
                出处
                
                    《中国糖尿病杂志》
                        
                                CAS
                                CSCD
                                北大核心
                        
                    
                        2008年第2期68-71,共4页
                    
                
                    Chinese Journal of Diabetes
     
            
                基金
                    国家重点基础研究发展计划资助项目(2006CB503908)