目的 研究不同糖耐量人群的血脂多糖水平及其与胰岛素抵抗、β细胞分泌功能的关系.方法 纳入新诊断的2型糖尿病患者(T2DM组)23例、糖耐量受损者(IGT组)21例和糖耐量正常者(NGT组)23名.血清脂多糖水平采用鲎变形细胞溶解物试验法测定,脂多糖toll样受体4(TLR4)在血浆单核细胞表面的表达采用流式细胞学方法测定,并测定一次高脂饮食后脂多糖在餐后0.5h及2h的变化.胰岛素抵抗指标采用稳态模型评估的胰岛素抵抗指数(HOMA-IR)来评估;β细胞分泌功能采用稳态模型评估的胰岛素β细胞功能指数( HOMA-β )/HOMA-IR、早期30 min内胰岛素变化与血糖变化的比值(ΔIns30/ΔG30)/HOMA-IR、120 min内胰岛素曲线下面积(AUCIns120min)/HOMA-IR评估.结果 各组在高脂饮食后的2h脂多糖均较空腹脂多糖显著升高[NGT:0.96(0.33,0.99)对0.62(0.22,0.64),IGT:1.08(0.53,1.22)对0.71(0.39,0.82),T2DM:1.23(0.62,1.43)对0.86(0.45,0.94),EU/ml,均P＜0.01].T2DM组及IGT组的空腹脂多糖、0.5h脂多糖、2h脂多糖和空腹TLR4均高于NGT组[空服脂多糖:0.86(0.45,0.94),0.71(0.39,0.82)对0.62(0.22,0.64),EU/ml;0.5h脂多糖:1.10(0.55,1.18),0.84(0.50,1.07)对0.73(0.31,0.76),EU/ml;2h脂多糖:1.23(0.62,1.43),1.08(0.53,1.22)对0.96(0.33,0.99),EU/ ml;空腹TLR4:36.96(17.22,55.19),30.34(15.00,45.18)对15.66(6.09,9.76),MIF/105细胞,均P＜0.01].相关分析显示,所有受试者的空腹脂多糖、120 min内脂多糖曲线下面积(AUCLPS120min)、空腹TLR4与胰岛素抵抗指标正相关(P＜0.05),与β细胞分泌功能指标负相关(P＜0.05).多重线性回归分析显示,空腹脂多糖是HOMA-IR的独立相关因素,0.5h脂多糖是(AIns30/ΔG30 )/HOMA-IR和AUCIns120min/HOMA-IR的独立相关因素.结论 不同糖耐量人群的空腹及高脂饮食后的脂多糖水平及空腹TLR4水平存在差异,并与胰岛素抵抗、β细胞分泌功能具有一定的相关性,提示脂多糖可能与血糖调节异常的发生发展有关.
目的 研究不同糖耐量人群的血脂多糖水平及其與胰島素牴抗、β細胞分泌功能的關繫.方法 納入新診斷的2型糖尿病患者(T2DM組)23例、糖耐量受損者(IGT組)21例和糖耐量正常者(NGT組)23名.血清脂多糖水平採用鱟變形細胞溶解物試驗法測定,脂多糖toll樣受體4(TLR4)在血漿單覈細胞錶麵的錶達採用流式細胞學方法測定,併測定一次高脂飲食後脂多糖在餐後0.5h及2h的變化.胰島素牴抗指標採用穩態模型評估的胰島素牴抗指數(HOMA-IR)來評估;β細胞分泌功能採用穩態模型評估的胰島素β細胞功能指數( HOMA-β )/HOMA-IR、早期30 min內胰島素變化與血糖變化的比值(ΔIns30/ΔG30)/HOMA-IR、120 min內胰島素麯線下麵積(AUCIns120min)/HOMA-IR評估.結果 各組在高脂飲食後的2h脂多糖均較空腹脂多糖顯著升高[NGT:0.96(0.33,0.99)對0.62(0.22,0.64),IGT:1.08(0.53,1.22)對0.71(0.39,0.82),T2DM:1.23(0.62,1.43)對0.86(0.45,0.94),EU/ml,均P＜0.01].T2DM組及IGT組的空腹脂多糖、0.5h脂多糖、2h脂多糖和空腹TLR4均高于NGT組[空服脂多糖:0.86(0.45,0.94),0.71(0.39,0.82)對0.62(0.22,0.64),EU/ml;0.5h脂多糖:1.10(0.55,1.18),0.84(0.50,1.07)對0.73(0.31,0.76),EU/ml;2h脂多糖:1.23(0.62,1.43),1.08(0.53,1.22)對0.96(0.33,0.99),EU/ ml;空腹TLR4:36.96(17.22,55.19),30.34(15.00,45.18)對15.66(6.09,9.76),MIF/105細胞,均P＜0.01].相關分析顯示,所有受試者的空腹脂多糖、120 min內脂多糖麯線下麵積(AUCLPS120min)、空腹TLR4與胰島素牴抗指標正相關(P＜0.05),與β細胞分泌功能指標負相關(P＜0.05).多重線性迴歸分析顯示,空腹脂多糖是HOMA-IR的獨立相關因素,0.5h脂多糖是(AIns30/ΔG30 )/HOMA-IR和AUCIns120min/HOMA-IR的獨立相關因素.結論 不同糖耐量人群的空腹及高脂飲食後的脂多糖水平及空腹TLR4水平存在差異,併與胰島素牴抗、β細胞分泌功能具有一定的相關性,提示脂多糖可能與血糖調節異常的髮生髮展有關.
목적 연구불동당내량인군적혈지다당수평급기여이도소저항、β세포분비공능적관계.방법 납입신진단적2형당뇨병환자(T2DM조)23례、당내량수손자(IGT조)21례화당내량정상자(NGT조)23명.혈청지다당수평채용후변형세포용해물시험법측정,지다당toll양수체4(TLR4)재혈장단핵세포표면적표체채용류식세포학방법측정,병측정일차고지음식후지다당재찬후0.5h급2h적변화.이도소저항지표채용은태모형평고적이도소저항지수(HOMA-IR)래평고;β세포분비공능채용은태모형평고적이도소β세포공능지수( HOMA-β )/HOMA-IR、조기30 min내이도소변화여혈당변화적비치(ΔIns30/ΔG30)/HOMA-IR、120 min내이도소곡선하면적(AUCIns120min)/HOMA-IR평고.결과 각조재고지음식후적2h지다당균교공복지다당현저승고[NGT:0.96(0.33,0.99)대0.62(0.22,0.64),IGT:1.08(0.53,1.22)대0.71(0.39,0.82),T2DM:1.23(0.62,1.43)대0.86(0.45,0.94),EU/ml,균P＜0.01].T2DM조급IGT조적공복지다당、0.5h지다당、2h지다당화공복TLR4균고우NGT조[공복지다당:0.86(0.45,0.94),0.71(0.39,0.82)대0.62(0.22,0.64),EU/ml;0.5h지다당:1.10(0.55,1.18),0.84(0.50,1.07)대0.73(0.31,0.76),EU/ml;2h지다당:1.23(0.62,1.43),1.08(0.53,1.22)대0.96(0.33,0.99),EU/ ml;공복TLR4:36.96(17.22,55.19),30.34(15.00,45.18)대15.66(6.09,9.76),MIF/105세포,균P＜0.01].상관분석현시,소유수시자적공복지다당、120 min내지다당곡선하면적(AUCLPS120min)、공복TLR4여이도소저항지표정상관(P＜0.05),여β세포분비공능지표부상관(P＜0.05).다중선성회귀분석현시,공복지다당시HOMA-IR적독립상관인소,0.5h지다당시(AIns30/ΔG30 )/HOMA-IR화AUCIns120min/HOMA-IR적독립상관인소.결론 불동당내량인군적공복급고지음식후적지다당수평급공복TLR4수평존재차이,병여이도소저항、β세포분비공능구유일정적상관성,제시지다당가능여혈당조절이상적발생발전유관.
Objective To investigate serum lipopolysaccharide (LPS) level in people with different glucose tolerances and to explore the relationship between LPS and insulin resistance/β-cell secretory function.Methods Sixty-seven subjects were recruited,including 23 with newly diagnosed type 2 diabetes ( T2DM),21 impaired glucose tolerance ( IGT),and 23 normal glucose tolerance (NGT).Serum LPS was assayed by limulus amebocyte lysate test ;expression of LPS toll-like receptor 4 (TLR4) on surface of plasma monocytes was measured by flow cytometric assays,and the changes of LPS levels by 0.5 hours and 2 hours after a high-fat diet were detected.Insulin resistance was evaluated by homeostasis model assessment for insulin resistance (HOMA-IR); β-cell secretory function was evaluated by homeostasis model assessment for β3 cell function ( HOMA-β )/HOMA-IR,increment in insulin in the first 30 minutes/increment in glucose in the first 30 minutes ( AIns30/ΔG30)/HOMA-IR,AUCIns120min/HOMA-IR.Results 2 h LPS levels after a high-fat diet were significantly higher than fasting LPS levels [ NGT:0.96(0.33,0.99)vs 0.62 (0.22,0.64),IGT:1.08(0.53,1.22)vs 0.71 (0.39,0.82),T2DM:1.23 (0.62,1.43)vs 0.86( 0.45,0.94 ),EU/ml,all P＜0.01 ].Fasting,0.5 h,and 2 h LPS levels and fasting TLR4 levels of T2 DM group and IGT group were respectively higher than those of NGT group [ fasting LPS:0.86( 0.45,0.94 ),0.71 ( 0.39,0.82 ) vs 0.62(0.22,0.64),EU/ml;0.5 h LPS:1.10(0.55,1.18),0.84(0.50,1.07) vs 0.73(0.31,0.76),EU/ml;2 h LPS:1.23(0.62,1.43),1.08(0.53,1.22)vs 0.96(0.33,0.99),EU/ml; fasting TLR4:36.96( 17.22,55.19),30.34 ( 15.00,45.18 )vs 15.66 (6.09,9.76),MIF/105 cells,all P＜0.01 ].Fasting LPS,AUCLPS 120 min,and fasting TLR4 were positively correlated with insulin resistance index and negatively correlated with β-cell secretory function index ( P＜0.05 ).Multiple linear regression analysis showed that fasting LPS was an independent correlative factor of HOMA-IR and 0.5 h LPS was an independent correlative factor of (AIns30/AG30)/HOMA-IR and AUCIns Ins120min/HOMA-IR.Conclusion People with different glucose tolerances show differed LPS levels and its receptor TLR4 levcls,both of which are correlated with insulin resistance and β-cell secretory function,suggesting that LPS is associated with the pathogenesis of abnormal glucose regulation.
