目的 了解2型糖尿病(T2DM)患者空腹血糖(FPG)水平与胰岛α及β细胞功能的相关性.方法 选择437例T2DM患者,按空腹血糖(FPG)水平分为三组:F1组:FPG≤6 mmol/L (73例),F2组:6 mmol/L< FPG≤7 mmol/L(103例),F3组:FPG>7mmol/L(261例),选择同期健康体检者30例作为对照组.联合进行口服葡萄糖耐量试验及胰岛素、胰高血糖素释放试验,比较各组间胰高血糖素、胰高血糖素/胰岛素、糖负荷后30 min胰岛素和血糖净增值的比值(△I30/△G30)、胰岛素曲线下面积(AUC1)等的变化,并对胰高血糖素与胰岛β细胞功能、糖化血红蛋白(HbA1c)等指标行相关性分析.结果 T2DM各组HbA1c、糖负荷后120 min血糖均明显高于对照组,差异有统计学意义(P<0.05).T2DM各组随着FPG的升高HbA1c、病程、糖负荷后120 min血糖呈现升高的趋势.F2组、F3组三酰甘油高于F1组、对照组,F3组低密度脂蛋白胆固醇高于F1组、F2组、对照组,差异有统计学意义(P<0.05).F1组糖负荷后60,120 min时,F2组糖负荷后30,60,120 min时,F3组糖负荷后30,60,120,180 min时胰高血糖素均高于对照组同时间点,差异有统计学意义(P<0.05).F2组糖负荷后60,120,180 min时,F3组空腹及糖负荷后30,60,120,180 min时胰高血糖素均高于F1组同时间点,差异有统计学意义(P<0.05).F3组空腹及糖负荷后30,60,120,180 min时胰高血糖素均高于F2组同时间点,差异有统计学意义(P<0.05).对照组胰高血糖素曲线下面积为9.5±0.3,F1组为9.7±0.2,F2组为9.9±0.2,F3组为10.2±0.3,呈逐渐升高趋势,各组间比较差异均有统计学意义(P<0.05).F1组空腹及糖负荷后30,60 min时,F2组空腹及糖负荷后30,60,120 min时,F3组空腹及糖负荷后30,60,120 min时胰高血糖素/胰岛素均高于对照组同时间点,差异有统计学意义(P<0.05).F2组空腹及糖负荷后60,120 min时,F3组空腹及糖负荷后30,60,120,180 min时胰高血糖素/胰岛素均高于F1组同时间点,差异有统计学意义(P<0.05).F3组糖负荷后30,60,120,180 min时胰高血糖素/胰岛素均高于F2组同时间点,差异有统计学意义(P<0.05).F2组和F3组稳态模型评估的胰岛素抵抗指数(HOMA-IR)均高于对照组和F1组,F3组高于F2组,差异有统计学意义(P<0.05).F2组和F3组胰岛素敏感性指数(ISI)均低于对照组和F1组,F3组低于F2组,差异有统计学意义(P<0.05).T2DM各组稳态模型评估的胰岛β细胞功能指数(HOMA-β)和△I30/△G30均低于对照组,T2DM各组呈逐渐降低的趋势,差异有统计学意义(P<0.05).F2组AUC1低于对照组,F3组AUC1低于对照组、F1组和F2组,差异有统计学意义(P<0.05).Pearson相关性分析结果显示,胰高血糖素与△I30/△G30、HOMA-β、体质量指数、ISI、AUC1呈负相关(r=-0.229,-0.153,-0.151,-0.146,-0.136,P<0.01或<0.05);与FPG、血糖曲线下面积(AUCG)、HbA1c、病程、HOMA-IR呈正相关(r=0.545,0.476,0.273,0.193,0.189,P<0.01).多元逐步回归分析结果显示,胰高血糖素与FPG、AUCG、HbA1c、病程呈正相关(P<0.01或<0.05),与△I30/△G30呈负相关(P<0.05).结论 T2DM患者随着FPG的升高,在胰岛β细胞分泌功能减低的同时,胰岛α细胞出现高分泌,对于FPG水平过高的患者,在保护胰岛β细胞功能的同时关注胰高血糖素的调控更容易使血糖达标.
目的 瞭解2型糖尿病(T2DM)患者空腹血糖(FPG)水平與胰島α及β細胞功能的相關性.方法 選擇437例T2DM患者,按空腹血糖(FPG)水平分為三組:F1組:FPG≤6 mmol/L (73例),F2組:6 mmol/L< FPG≤7 mmol/L(103例),F3組:FPG>7mmol/L(261例),選擇同期健康體檢者30例作為對照組.聯閤進行口服葡萄糖耐量試驗及胰島素、胰高血糖素釋放試驗,比較各組間胰高血糖素、胰高血糖素/胰島素、糖負荷後30 min胰島素和血糖淨增值的比值(△I30/△G30)、胰島素麯線下麵積(AUC1)等的變化,併對胰高血糖素與胰島β細胞功能、糖化血紅蛋白(HbA1c)等指標行相關性分析.結果 T2DM各組HbA1c、糖負荷後120 min血糖均明顯高于對照組,差異有統計學意義(P<0.05).T2DM各組隨著FPG的升高HbA1c、病程、糖負荷後120 min血糖呈現升高的趨勢.F2組、F3組三酰甘油高于F1組、對照組,F3組低密度脂蛋白膽固醇高于F1組、F2組、對照組,差異有統計學意義(P<0.05).F1組糖負荷後60,120 min時,F2組糖負荷後30,60,120 min時,F3組糖負荷後30,60,120,180 min時胰高血糖素均高于對照組同時間點,差異有統計學意義(P<0.05).F2組糖負荷後60,120,180 min時,F3組空腹及糖負荷後30,60,120,180 min時胰高血糖素均高于F1組同時間點,差異有統計學意義(P<0.05).F3組空腹及糖負荷後30,60,120,180 min時胰高血糖素均高于F2組同時間點,差異有統計學意義(P<0.05).對照組胰高血糖素麯線下麵積為9.5±0.3,F1組為9.7±0.2,F2組為9.9±0.2,F3組為10.2±0.3,呈逐漸升高趨勢,各組間比較差異均有統計學意義(P<0.05).F1組空腹及糖負荷後30,60 min時,F2組空腹及糖負荷後30,60,120 min時,F3組空腹及糖負荷後30,60,120 min時胰高血糖素/胰島素均高于對照組同時間點,差異有統計學意義(P<0.05).F2組空腹及糖負荷後60,120 min時,F3組空腹及糖負荷後30,60,120,180 min時胰高血糖素/胰島素均高于F1組同時間點,差異有統計學意義(P<0.05).F3組糖負荷後30,60,120,180 min時胰高血糖素/胰島素均高于F2組同時間點,差異有統計學意義(P<0.05).F2組和F3組穩態模型評估的胰島素牴抗指數(HOMA-IR)均高于對照組和F1組,F3組高于F2組,差異有統計學意義(P<0.05).F2組和F3組胰島素敏感性指數(ISI)均低于對照組和F1組,F3組低于F2組,差異有統計學意義(P<0.05).T2DM各組穩態模型評估的胰島β細胞功能指數(HOMA-β)和△I30/△G30均低于對照組,T2DM各組呈逐漸降低的趨勢,差異有統計學意義(P<0.05).F2組AUC1低于對照組,F3組AUC1低于對照組、F1組和F2組,差異有統計學意義(P<0.05).Pearson相關性分析結果顯示,胰高血糖素與△I30/△G30、HOMA-β、體質量指數、ISI、AUC1呈負相關(r=-0.229,-0.153,-0.151,-0.146,-0.136,P<0.01或<0.05);與FPG、血糖麯線下麵積(AUCG)、HbA1c、病程、HOMA-IR呈正相關(r=0.545,0.476,0.273,0.193,0.189,P<0.01).多元逐步迴歸分析結果顯示,胰高血糖素與FPG、AUCG、HbA1c、病程呈正相關(P<0.01或<0.05),與△I30/△G30呈負相關(P<0.05).結論 T2DM患者隨著FPG的升高,在胰島β細胞分泌功能減低的同時,胰島α細胞齣現高分泌,對于FPG水平過高的患者,在保護胰島β細胞功能的同時關註胰高血糖素的調控更容易使血糖達標.
목적 료해2형당뇨병(T2DM)환자공복혈당(FPG)수평여이도α급β세포공능적상관성.방법 선택437례T2DM환자,안공복혈당(FPG)수평분위삼조:F1조:FPG≤6 mmol/L (73례),F2조:6 mmol/L< FPG≤7 mmol/L(103례),F3조:FPG>7mmol/L(261례),선택동기건강체검자30례작위대조조.연합진행구복포도당내량시험급이도소、이고혈당소석방시험,비교각조간이고혈당소、이고혈당소/이도소、당부하후30 min이도소화혈당정증치적비치(△I30/△G30)、이도소곡선하면적(AUC1)등적변화,병대이고혈당소여이도β세포공능、당화혈홍단백(HbA1c)등지표행상관성분석.결과 T2DM각조HbA1c、당부하후120 min혈당균명현고우대조조,차이유통계학의의(P<0.05).T2DM각조수착FPG적승고HbA1c、병정、당부하후120 min혈당정현승고적추세.F2조、F3조삼선감유고우F1조、대조조,F3조저밀도지단백담고순고우F1조、F2조、대조조,차이유통계학의의(P<0.05).F1조당부하후60,120 min시,F2조당부하후30,60,120 min시,F3조당부하후30,60,120,180 min시이고혈당소균고우대조조동시간점,차이유통계학의의(P<0.05).F2조당부하후60,120,180 min시,F3조공복급당부하후30,60,120,180 min시이고혈당소균고우F1조동시간점,차이유통계학의의(P<0.05).F3조공복급당부하후30,60,120,180 min시이고혈당소균고우F2조동시간점,차이유통계학의의(P<0.05).대조조이고혈당소곡선하면적위9.5±0.3,F1조위9.7±0.2,F2조위9.9±0.2,F3조위10.2±0.3,정축점승고추세,각조간비교차이균유통계학의의(P<0.05).F1조공복급당부하후30,60 min시,F2조공복급당부하후30,60,120 min시,F3조공복급당부하후30,60,120 min시이고혈당소/이도소균고우대조조동시간점,차이유통계학의의(P<0.05).F2조공복급당부하후60,120 min시,F3조공복급당부하후30,60,120,180 min시이고혈당소/이도소균고우F1조동시간점,차이유통계학의의(P<0.05).F3조당부하후30,60,120,180 min시이고혈당소/이도소균고우F2조동시간점,차이유통계학의의(P<0.05).F2조화F3조은태모형평고적이도소저항지수(HOMA-IR)균고우대조조화F1조,F3조고우F2조,차이유통계학의의(P<0.05).F2조화F3조이도소민감성지수(ISI)균저우대조조화F1조,F3조저우F2조,차이유통계학의의(P<0.05).T2DM각조은태모형평고적이도β세포공능지수(HOMA-β)화△I30/△G30균저우대조조,T2DM각조정축점강저적추세,차이유통계학의의(P<0.05).F2조AUC1저우대조조,F3조AUC1저우대조조、F1조화F2조,차이유통계학의의(P<0.05).Pearson상관성분석결과현시,이고혈당소여△I30/△G30、HOMA-β、체질량지수、ISI、AUC1정부상관(r=-0.229,-0.153,-0.151,-0.146,-0.136,P<0.01혹<0.05);여FPG、혈당곡선하면적(AUCG)、HbA1c、병정、HOMA-IR정정상관(r=0.545,0.476,0.273,0.193,0.189,P<0.01).다원축보회귀분석결과현시,이고혈당소여FPG、AUCG、HbA1c、병정정정상관(P<0.01혹<0.05),여△I30/△G30정부상관(P<0.05).결론 T2DM환자수착FPG적승고,재이도β세포분비공능감저적동시,이도α세포출현고분비,대우FPG수평과고적환자,재보호이도β세포공능적동시관주이고혈당소적조공경용역사혈당체표.
Objective To investigate the relationship between fasting plasma glucose (FPG) and islet α-cell and β-cell function in patients with type 2 diabetes mellitus (T2DM).Methods Four hundred and thirty-seven patients with T2DM were divided into 3 groups according to the level of FPG:F1 group:FPG ≤ 6 mmol/L (73 cases),F2 group:6 mmol/L < FPG ≤ 7 mmol/L (103 cases),and F3 group:FPG > 7mmol/L (261 cases),and 30 cases of healthy people were selected as control group.Oral glucose tolerance test,insulin releasing test and glucagon releasing test were performed to observe the differences of glucagon,glucagon/ insulin,the ratio of 30 min insulin and blood glucose value after glucose load (△ I30/△ G30),and the area under curve of insulin (AUC1) among the 4 groups and the correlation analysis was performed between glucagon and other indicators.Results Glycosylated hemoglobin (HbA1c),plasma glucose 120 at min after glucose load in F1,F2 and F3 group were significantly higher than those in control group,and there were statistical differences (P <0.05).In F1,F2,F3 group,with the increase of the HbA1c,the course of disease and plasma glucose at 120 min after glucose load showed increasing trend.The triglyceride in F2 group and F3 group was significantly higher than that in F1 group and control group,and low density lipoprotein cholesterol in F3 group was significantly higher than that in F1 group,F2 group and control group,and there were statistical differences (P < 0.05).The glucagon at 60,120 min after glucose load in F1 group,30,60,120 min after glucose load in F2 group,and 30,60,120,180 min after glucose load in F3 group was significantly higher than that in control group,and there were statistical differences (P < 0.05).The glucagon at 60,120,180 min after glucose load in F2 group,at fasting and 30,60,120,180 rain after glucose load in F3 group was significantly higher than that in F1 group,and there were statistical differences (P < 0.05).The glucagon at fasting and 30,60,120,180 min after glucose load in F3 group was significantly higher than that in F2 group,and there were statistical differences (P < 0.05).The area under curve of glucagon in control group was 9.5 ±0.3,in F1 group was 9.7 ± 0.2,in F2 group was 9.9 ± 0.2,in F3 group was 10.2 ± 0.3,and there were statistical differences among the 4 groups (P < 0.05).The glucagon/insulin at fasting and 30,60 min after glucose load in F1 groups,fasting and 30,60,120 min after glucose load in F2 group,fasting and 30,60,120 min after glucose load in F3 group was significantly higher than that in control group,and there were statistical differences (P< 0.05).The glucagon/insulin at fasting and 60,120 min after glucose load in F2 group,fasting and 30,60,120,180 min after glucose load in F3 group was significantly higher than that in F1 group,and there were statistical differences (P < 0.05).The glucagon/insulin 30,60,120,180 min after glucose load in F3 group was significantly higher than that in F2 group,and there were statistical differences (P< 0.05).The homeostasis model of assessment for insulin resistance index (HOMA-IR) in F2 group and F3 group was significantly higher than that in control group and F1 group,in F3 group was significantly higher than that in F2 group,and there were statistical differences (P< 0.05).The insulin sensitivity index (ISI) in F2 group and F3 group was significantly lower than that in control group and F1 group,in F3 group was significantly lower than that in F2 group,and there were statistical differences (P < 0.05).The homeostasis model of assessment for islet β-cell function index (HOMA-β) and △I30/△G30 in F1,F2,F3 group were significantly lower than those in control group,and there were statistical differences (P < 0.05).The AUC1 in F2 group was significantly lower than that in control group,and AUC1 in F3 group was significantly lower than that in control group,F1 group and F2 group,there were statistical differences (P <0.05).The results of Pearson correlation analysis showed there was negative correlation between glucagon and △I30/△G30,HOMA-β,body mass index,ISI,AUC1 (r =-0.229,-0.153,-0.151,-0.146,-0.136,P<0.01 or <0.05),and there was positive correlation between glucagon and FPG,area under curve of glucose (AUCG),HbA1c,course of disease and HOMA-IR (r =0.545,0.476,0.273,0.193,0.189,P < 0.01).The results of multiplestepwise regression analysis showed there was positive correlation between glucagon and FPG,AUCG,HbA1c,course of disease (P <0.01 or <0.05),and there was negative correlation between glucagon and △I30/△ G30 (P < 0.05).Conclusions Islet β-cell function is decreased with the increasing of FPG,while islet α-cell function is increased,especially in those with higher levels of FPG.Regulation of glucagon should be concerned to make the blood glucose target easier to reach,at the same time of protecting β-cell function.