中华临床医师杂志(电子版)
中華臨床醫師雜誌(電子版)
중화림상의사잡지(전자판)
CHINESE JOURNAL OF CLINICIANS(ELECTRONIC VERSION)
2013年
13期
5798-5801
,共4页
徐倩%张方华%许爱梅%王秀秀%姚民秀
徐倩%張方華%許愛梅%王秀秀%姚民秀
서천%장방화%허애매%왕수수%요민수
糖尿病,2型%二甲双胍%抵抗素%胰岛素样生长因子Ⅰ
糖尿病,2型%二甲雙胍%牴抗素%胰島素樣生長因子Ⅰ
당뇨병,2형%이갑쌍고%저항소%이도소양생장인자Ⅰ
Diabetes mellitus,type 2%Metformin%Resistin%Insulin-like growth factorⅠ
目的:检测新诊断的肥胖2型糖尿病人群经单用二甲双胍治疗前后抵抗素、胰岛素样生长因子Ⅰ( IGF-Ⅰ)及炎症因子的变化,探讨二甲双胍改善胰岛素抵抗及预防肿瘤发生的分子机制。方法选取新诊断的肥胖2型糖尿病人56例及健康对照50例,经饮食及运动治疗1周后给予二甲双胍1500 mg/d,治疗3个月,给药前后分别抽取空腹静脉血,测定空腹血糖、空腹胰岛素、糖化血红蛋白、抵抗素、IGF-Ⅰ、白细胞介素-6(IL-6)和超敏的C反应蛋白(sCRP),应用稳态模型评估法评价胰岛素抵抗指数(HOMA-IR)。治疗前后的比较及组间的比较采用t检验及单因素方差分析。多因素的分析采用多元回归分析。结果二甲双胍治疗前后空腹血糖、空腹胰岛素、HOMA-IR、糖化血红蛋白、抵抗素、IGF-Ⅰ、IL-6和sCRP 明显下降( P<0.05),但仍高于正常对照组( P<0.05)。抵抗素、IL-6和sCRP与胰岛素抵抗指数呈正相关( r=0.95,0.89,0.78,P<0.01),是后者的独立影响因素(β=1.91,0.148,1.6,P=0.000);空腹胰岛素与IGF-Ⅰ呈正相关(r=0.91,P<0.01),是IGF-Ⅰ的独立影响因素(β=4.30,P=0.000)。结论新诊断的肥胖2型糖尿病给予二甲双胍治疗后可能通过降低抵抗素及炎症因子的水平,改善胰岛素抵抗,从而降低了血清胰岛素和IGF-Ⅰ的水平。
目的:檢測新診斷的肥胖2型糖尿病人群經單用二甲雙胍治療前後牴抗素、胰島素樣生長因子Ⅰ( IGF-Ⅰ)及炎癥因子的變化,探討二甲雙胍改善胰島素牴抗及預防腫瘤髮生的分子機製。方法選取新診斷的肥胖2型糖尿病人56例及健康對照50例,經飲食及運動治療1週後給予二甲雙胍1500 mg/d,治療3箇月,給藥前後分彆抽取空腹靜脈血,測定空腹血糖、空腹胰島素、糖化血紅蛋白、牴抗素、IGF-Ⅰ、白細胞介素-6(IL-6)和超敏的C反應蛋白(sCRP),應用穩態模型評估法評價胰島素牴抗指數(HOMA-IR)。治療前後的比較及組間的比較採用t檢驗及單因素方差分析。多因素的分析採用多元迴歸分析。結果二甲雙胍治療前後空腹血糖、空腹胰島素、HOMA-IR、糖化血紅蛋白、牴抗素、IGF-Ⅰ、IL-6和sCRP 明顯下降( P<0.05),但仍高于正常對照組( P<0.05)。牴抗素、IL-6和sCRP與胰島素牴抗指數呈正相關( r=0.95,0.89,0.78,P<0.01),是後者的獨立影響因素(β=1.91,0.148,1.6,P=0.000);空腹胰島素與IGF-Ⅰ呈正相關(r=0.91,P<0.01),是IGF-Ⅰ的獨立影響因素(β=4.30,P=0.000)。結論新診斷的肥胖2型糖尿病給予二甲雙胍治療後可能通過降低牴抗素及炎癥因子的水平,改善胰島素牴抗,從而降低瞭血清胰島素和IGF-Ⅰ的水平。
목적:검측신진단적비반2형당뇨병인군경단용이갑쌍고치료전후저항소、이도소양생장인자Ⅰ( IGF-Ⅰ)급염증인자적변화,탐토이갑쌍고개선이도소저항급예방종류발생적분자궤제。방법선취신진단적비반2형당뇨병인56례급건강대조50례,경음식급운동치료1주후급여이갑쌍고1500 mg/d,치료3개월,급약전후분별추취공복정맥혈,측정공복혈당、공복이도소、당화혈홍단백、저항소、IGF-Ⅰ、백세포개소-6(IL-6)화초민적C반응단백(sCRP),응용은태모형평고법평개이도소저항지수(HOMA-IR)。치료전후적비교급조간적비교채용t검험급단인소방차분석。다인소적분석채용다원회귀분석。결과이갑쌍고치료전후공복혈당、공복이도소、HOMA-IR、당화혈홍단백、저항소、IGF-Ⅰ、IL-6화sCRP 명현하강( P<0.05),단잉고우정상대조조( P<0.05)。저항소、IL-6화sCRP여이도소저항지수정정상관( r=0.95,0.89,0.78,P<0.01),시후자적독립영향인소(β=1.91,0.148,1.6,P=0.000);공복이도소여IGF-Ⅰ정정상관(r=0.91,P<0.01),시IGF-Ⅰ적독립영향인소(β=4.30,P=0.000)。결론신진단적비반2형당뇨병급여이갑쌍고치료후가능통과강저저항소급염증인자적수평,개선이도소저항,종이강저료혈청이도소화IGF-Ⅰ적수평。
Objective To investigate molecular mechanisms of metformin improving insulin resistance and preventing carcinogenesis by measuring resistin ,insulin-like growth factor-Ⅰ( IGF-Ⅰ) and markers of inflammation in newly diagnosed obese type 2 diabetes with metformin therapy .Methods 56 newly diagnosed obese type 2 diabetes who were treated with metformin 1500 mg per day for 3 months after dietary and exercises one week and 50 healthy people as control were selected .Fasting blood glucose ,insulin,hemoglobin A1c,resistin,IGF-Ⅰ,interleukin-6(IL-6)and hypersensitivity C reactive protein (sCRP)were measured.Homeostasis model assessment was used to evaluate the basal insulin resistance ( HOMA-IR ) , t-test and one-way variance analysis were used in the study . Results Fasting blood glucose,insulin,hemoglobin A1c,resistin,IGF-Ⅰ,IL-6,sCRP and HOMA-IR were decreased in type 2 diabetes with metformin 1500 mg per day for 3 months(P<0.05),but were higher than in healthy people (P<0.05).Resistin,IL-6 and sCRP were positively correlated with HOMA-IR(r=0.95,0.89,0.78,P<0.01), which was independent factors of the latter (β=1.91,0.148,1.6,P=0.000).A significantly positive relationship were shown between fasting blood insulin and IGF-Ⅰ( r=0.91 ,P<0.01 ) and the former was independent factors of the latter(β=4.30,P=0.000).Conclusion Metformin therapy may be possible to reduce the levels of resistin and inflammatory factor in newly diagnosed obesity type 2 diabetes , improve insunlin resistance , thereby decrease the levels of serum insulin and IGF-Ⅰ.