CAJ | 학술논문

目的探讨2型糖尿病(T2DM)患者胰岛β细胞功能衰竭与心功能不全的临床表现特点及相关激素的改变,寻找针对糖尿病心功能不全的干预靶点.方法选取2008年1月至4月四川省人民医院门诊及住院部收治的T2DM患者96例(A组)、健康体检者35名(B组,健康对照).将A组按病程和心力衰竭症状分为:新诊断及病程<2年T2DM 患者33例(A1组)、病程>2年未出现临床显性心力衰竭症状和体征的T2DM患者32例(A2组)、病程>2年且已出现临床显性心力衰竭症状和体征的T2DM 患者31例(A3组).入选者均测空腹血糖(FPG)、胰岛素(FINS)、真胰岛素(TI)、胰岛素原(PI)1次,注射胰岛素治疗A组患者测空腹C肽1次,以胰岛素分泌指数 (Homa-Is)判定胰岛β细胞分泌功能;所有入选者均测定脑钠素(BNP)并采用心脏彩色多普勒测定左室射血分数(LVEF)、二尖瓣口舒张早期流速峰值E峰/舒张晚期流速峰值A峰(E/A)、舒张早期波e峰/舒张晚期波a峰(e/a)、峰值肺静脉血流收缩期S波/峰值肺静脉舒张早中期D波(S/D)以判定心脏功能.应用方差分析进行各组数据分析比较.结果随着T2DM病程的进展,Homa-Is进行性下降(B组为110.0±76.3、A1组为45.0±22.7、A2组为15.0±14.0、A3组为5.8±2.4,F=6.34,P<0.05),A3组TI及PI与其余各组比较有明显的降低.BNP随胰岛β细胞分泌功能的降低出现了显著增高[B组为(75±19)ng/L、A1组为(810±185)ng/L、A2组为(1060±264)ng/L、A3组为(2071±785)ng/L,F=8.89,P<0.05];心脏彩超T2DM组较健康对照组E/A 、e/a 、S/D、LVEF均有明显下降,随着胰岛β细胞分泌功能下降差异愈明显.结论随着T2DM病程延长及胰岛β细胞功能逐渐衰竭,真胰岛素、胰岛素原分泌水平减少及心肌舒张顺应性减低和收缩力下降,使得心脏泵功能发生与供能相关的代谢障碍,从而影响和加重心力衰竭.
목적 탐토2형당뇨병(T2DM)환자이도β세포공능쇠갈여심공능불전적림상표현특점급상관격소적개변,심조침대당뇨병심공능불전적간예파점.방법 선취2008년1월지4월사천성인민의원문진급주원부수치적T2DM환자96례(A조)、건강체검자35명(B조,건강대조).장A조안병정화심력쇠갈증상분위:신진단급병정<2년T2DM 환자33례(A1조)、병정>2년미출현림상현성심력쇠갈증상화체정적T2DM환자32례(A2조)、병정>2년차이출현림상현성심력쇠갈증상화체정적T2DM 환자31례(A3조).입선자균측공복혈당(FPG)、이도소(FINS)、진이도소(TI)、이도소원(PI)1차,주사이도소치료A조환자측공복C태1차,이이도소분비지수 (Homa-Is)판정이도β세포분비공능;소유입선자균측정뇌납소(BNP)병채용심장채색다보륵측정좌실사혈분수(LVEF)、이첨판구서장조기류속봉치E봉/서장만기류속봉치A봉(E/A)、서장조기파e봉/서장만기파a봉(e/a)、봉치폐정맥혈류수축기S파/봉치폐정맥서장조중기D파(S/D)이판정심장공능.응용방차분석진행각조수거분석비교.결과 수착T2DM병정적진전,Homa-Is진행성하강(B조위110.0±76.3、A1조위45.0±22.7、A2조위15.0±14.0、A3조위5.8±2.4,F=6.34,P<0.05),A3조TI급PI여기여각조비교유명현적강저.BNP수이도β세포분비공능적강저출현료현저증고[B조위(75±19)ng/L、A1조위(810±185)ng/L、A2조위(1060±264)ng/L、A3조위(2071±785)ng/L,F=8.89,P<0.05];심장채초T2DM조교건강대조조E/A 、e/a 、S/D、LVEF균유명현하강,수착이도β세포분비공능하강차이유명현.결론 수착T2DM병정연장급이도β세포공능축점쇠갈,진이도소、이도소원분비수평감소급심기서장순응성감저화수축력하강,사득심장빙공능발생여공능상관적대사장애,종이영향화가중심력쇠갈.
Objective To investigate the clinical features and related hormone changes of diabetic cardiac insufficiency and pancreatic β-cell dysfunction in type 2 diabetes mellitus(T2DM). MethodsFrom January to April 2008,96 patients with T2DM(group A) and 35 healthy volunteers with a normal glucose tolerance (NGT) (group B) were enrolled in this study. According to the course of T2DM and symptom of heart failure, the patients in group A were divided into three groups: group A1: newly-diagnosed T2DM or course of T2DM<2 years, n=33; group A2: course of T2DM>2 years without obvious signs and symptoms of heart failure, n=32; group A3: course of T2DM>2 years with obvious clinical signs and symptoms of heart failure, n=31. The serum fasting plasma glucose (FPG), fasting insulin(FINS), true insulin(TI), proinsulin(PI) and brain natriuretic peptide(BNP) were detected in all the subjects. The ratio between early diastolic peak flow velocity and atrium peak flow velocity(E/A), the lateral wall of mitral annular movement(e/a), pulmonary venous peak systolic velocities and diastolic velocities (S/D) and left ventricular ejection fraction(LVEF) stage in all subjects were examined by echocardiogram. Variance analysis was used for data analysis among the 4 groups. Results The Homa-Is decreased with the progression of T2DM (group B: 110.0±76.3, group A1:45.0±22.7, group A2: 15.0±14.0, group A3: 5.8±2.4; F=6.34,P<0.05); it indicated that the secretary function of β-cell declined significantly with the progress of T2DM. The serum level of BNP was significantly increased accompanied the function declines of pancreatic β-cell (group B: (75±19) ng/L, group A1:(810±185) ng/L, group A2:(1060±264) ng/L, group A3: (2071±785) ng/L; F=8.89,P<0.05). The serum level of TI and PI in group A3 were all significantly lower than those in group B, A1 and A2 (all P<0.05). The values of E/A, e/a, S/D and LVEF in group A were all significantly lower than those in group B (all P<0.05). Conclusion With the functional declines of pancreatic β-cell in T2DM, the myocardial contractility and diastolic function declines, meanwhile the TI and PI secretion reduces, and these changes finally induce metabolic disorders which can aggravate heart failure.