中国综合临床
中國綜閤臨床
중국종합림상
CLINICAL MEDICINE OF CHINA
2010年
5期
507-510
,共4页
2型糖尿病%胰岛素%强化治疗%胰岛素抵抗%胰岛β细胞功能
2型糖尿病%胰島素%彊化治療%胰島素牴抗%胰島β細胞功能
2형당뇨병%이도소%강화치료%이도소저항%이도β세포공능
Type 2 diabetes%Insulin%Intensive treatment%Insulin resistance%Islet β cell function
目的 评价三种短期胰岛素强化治疗改善不同胰岛素抵抗状态初诊2型糖尿病(T2DM)患者胰岛β细胞功能的效果.方法 初诊T2DM患者98例,分为存在胰岛素抵抗(IR)组(HOMA-IR≥5)和不存在胰岛素抵抗(Non-IR)组(HOMA-IR＜5);分别接受持续胰岛素皮下输注(CSⅡ)、门冬胰岛素加甘精胰岛素(glar)、门冬胰岛素30注射液(aspart 30)强化治疗,IR-CSⅡ组20例,IR-glar组22例,IR-aspart 30组23例;Non-IR-CSⅡ组10例,Non-IR-glar组12例,Non-IR-aspart 30组11例.测定6组治疗2周前后空腹血糖(FPG)、空腹C肽(C-P)、餐后2 h血糖(2 hPG),采用空腹C-P水平计算β细胞功能指数[HOMA-islet(C-P)]和胰岛素抵抗指数[HOMA-IR(C-P)].结果血糖达标时间、胰岛素用量、低血糖发生频率在CSⅡ组少于glar组和aspart 30组(P＜0.05或＜0.01),glar组与aspart 30组比较差异无统计学意义(P均＞0.05).达标时Non-IR组胰岛素日用量低于同种治疗方式的IR组(P均＜0.01),△HOMA-islet(C-P)高于IR组(P均＜0.05),△HOMA-IR(C-P)低于IR组(P＜0.05);CSⅡ组△HOMA-IR(C-P)(IR组1.79±0.15,Non-IR组1.51±0.09)和△HOMA-islet(C-P)(IR组4.01±0.21,Non-IR组4.35±0.23)高于glar组(IR组1.63±0.21、3.86±0.12,Non-IR组1.40±0.19、4.03±0.18)和aspart 30组(IR组1.61±0.13、3.88±0.32,Non-IR组1.42±0.11、4.01±0.14,P＜0.05或＜0.01).结论 三种胰岛素强化治疗方式均可改善伴有高血糖的初诊2型糖尿病患者胰岛β细胞功能,减轻胰岛素抵抗,尤以CSⅡ效果更好.但有明显胰岛素抵抗的患者治疗效果欠佳.
目的 評價三種短期胰島素彊化治療改善不同胰島素牴抗狀態初診2型糖尿病(T2DM)患者胰島β細胞功能的效果.方法 初診T2DM患者98例,分為存在胰島素牴抗(IR)組(HOMA-IR≥5)和不存在胰島素牴抗(Non-IR)組(HOMA-IR＜5);分彆接受持續胰島素皮下輸註(CSⅡ)、門鼕胰島素加甘精胰島素(glar)、門鼕胰島素30註射液(aspart 30)彊化治療,IR-CSⅡ組20例,IR-glar組22例,IR-aspart 30組23例;Non-IR-CSⅡ組10例,Non-IR-glar組12例,Non-IR-aspart 30組11例.測定6組治療2週前後空腹血糖(FPG)、空腹C肽(C-P)、餐後2 h血糖(2 hPG),採用空腹C-P水平計算β細胞功能指數[HOMA-islet(C-P)]和胰島素牴抗指數[HOMA-IR(C-P)].結果血糖達標時間、胰島素用量、低血糖髮生頻率在CSⅡ組少于glar組和aspart 30組(P＜0.05或＜0.01),glar組與aspart 30組比較差異無統計學意義(P均＞0.05).達標時Non-IR組胰島素日用量低于同種治療方式的IR組(P均＜0.01),△HOMA-islet(C-P)高于IR組(P均＜0.05),△HOMA-IR(C-P)低于IR組(P＜0.05);CSⅡ組△HOMA-IR(C-P)(IR組1.79±0.15,Non-IR組1.51±0.09)和△HOMA-islet(C-P)(IR組4.01±0.21,Non-IR組4.35±0.23)高于glar組(IR組1.63±0.21、3.86±0.12,Non-IR組1.40±0.19、4.03±0.18)和aspart 30組(IR組1.61±0.13、3.88±0.32,Non-IR組1.42±0.11、4.01±0.14,P＜0.05或＜0.01).結論 三種胰島素彊化治療方式均可改善伴有高血糖的初診2型糖尿病患者胰島β細胞功能,減輕胰島素牴抗,尤以CSⅡ效果更好.但有明顯胰島素牴抗的患者治療效果欠佳.
목적 평개삼충단기이도소강화치료개선불동이도소저항상태초진2형당뇨병(T2DM)환자이도β세포공능적효과.방법 초진T2DM환자98례,분위존재이도소저항(IR)조(HOMA-IR≥5)화불존재이도소저항(Non-IR)조(HOMA-IR＜5);분별접수지속이도소피하수주(CSⅡ)、문동이도소가감정이도소(glar)、문동이도소30주사액(aspart 30)강화치료,IR-CSⅡ조20례,IR-glar조22례,IR-aspart 30조23례;Non-IR-CSⅡ조10례,Non-IR-glar조12례,Non-IR-aspart 30조11례.측정6조치료2주전후공복혈당(FPG)、공복C태(C-P)、찬후2 h혈당(2 hPG),채용공복C-P수평계산β세포공능지수[HOMA-islet(C-P)]화이도소저항지수[HOMA-IR(C-P)].결과혈당체표시간、이도소용량、저혈당발생빈솔재CSⅡ조소우glar조화aspart 30조(P＜0.05혹＜0.01),glar조여aspart 30조비교차이무통계학의의(P균＞0.05).체표시Non-IR조이도소일용량저우동충치료방식적IR조(P균＜0.01),△HOMA-islet(C-P)고우IR조(P균＜0.05),△HOMA-IR(C-P)저우IR조(P＜0.05);CSⅡ조△HOMA-IR(C-P)(IR조1.79±0.15,Non-IR조1.51±0.09)화△HOMA-islet(C-P)(IR조4.01±0.21,Non-IR조4.35±0.23)고우glar조(IR조1.63±0.21、3.86±0.12,Non-IR조1.40±0.19、4.03±0.18)화aspart 30조(IR조1.61±0.13、3.88±0.32,Non-IR조1.42±0.11、4.01±0.14,P＜0.05혹＜0.01).결론 삼충이도소강화치료방식균가개선반유고혈당적초진2형당뇨병환자이도β세포공능,감경이도소저항,우이CSⅡ효과경호.단유명현이도소저항적환자치료효과흠가.
Objective To investigate the effects on the improvement of the function of islet β cell by three intensive insulin treatments on newly diagnosed type 2 diabetes(T2D) in different insulin resistant status.Methods Ninety-eight patients of newly diagnosed T2D were divided into two groups:group with overt insulin resistant status ( IR group) ( HOMA-IR ≥ 5 ); group without overt insulin resistant status ( Non-IR group) ( HOMA-IR ＜ 5).According to the condition of patient,there were six subgroups:IR-CSⅡ group ( n = 20 ); IR-glar group ( n = 22 );IR-aspart 30 group (n=23); Non-IR-CSⅡ group (n= 10); Non-IR-glar group (n=12); Non-IR-aspart 30 group (n = 11 ).Subgroups were treated with continuous subcutaneous insulin injection (CSⅡ group),insulin aspart plus insulin glargine ( glar group),and insulin aspart 30 injection ( aspart 30 group) for two weeks,respectively.The levels of fasting plasma glucose (FPG) ,fasting C-peptide(C-P) ,2 h plasma glucose (2 hPG) were measured and homeostasis model assessments of beta cell (HOMA-β) and homeostasis model assessments of insulin resistance ( HOMA-IR) were calculated using fasting C-P.Results The time of blood glucose recover,insulin dosage and the incidence of hypoglycemia of CSⅡ group were lower than those of the glar group and aspart 30 group( P ＜ 0.05 and P ＜0.01 ,respectively).However,there were no significant difference between the glar-group and aspart 30 group ( P ＞ 0.05 ).The insulin dosage of Non-IR-subgroups was significantly lower than the IR-subgroups ( P ＜ 0.01 ).The △HOMA-IR(C-P) of Non-IR-subgroups was lower than the IR-subgroups ( P ＜ 0.05 ).The △HOMA-islet(C-P) of the Non-IR-subgroups was higher than the IR-subgroups ( P ＜ 0.05 ).The △HOMA-IR(C-P) ( 1.79 ± 0.15 and 1.51 ±0.09 in IR and non-IR group,respectively) and △HOMA-islet(C-P) (4.01 ±0.21 and 4.35 ±0.23 in IR and Non-IR group,respectively) of the CSⅡ group were higher than those of the glar group (1.63 ± 0.21 and 1.40 ±0.19 of △HOMA-IR (C-P) and 3.86 ± 0.12 and 4.03 ± 0.18 of △HOMA-islet(C-P) in IR and Non-IR group,respectively) and aspart 30 group ( 1.61 ± 0.13 and 1.42 ± 0.1 1 ) △HOMA-islet (C-P) and 3.88 ± 0.32 and 4.01 ±0.14of△HOMA-islet(C-P)inIRandNon-IRgroup,respeetively)(P＜0.05).Conclusions Thethree intensive insulin treatments for newly diagnosed T2D accompanied with high blood glucose may improve the function of β cell and alleviate insulin resistance,especially the CSⅡ.However,the efficacy on T2D with overt insulin resistant status is limited.
