胎儿生长受限仔鼠脂肪组织中葡萄糖转运蛋白4的表达和细胞转位变化

Objective To investigate the effects of fetal growth restriction (FGR) on the expressions and translocation of glucose transporter 4 (GLUT4) in adipose tissue of male offsprings and its relationship with insulin resistance in FGR. Methods Male 8-week-old offspring from maternal with protein-malnutrition or normal diet were studied. The weight of rats at 8 weeks of age were obtained and insulin resistance index (IRI) was examined at 4 weeks and 8 weeks of age. Perinephric fat pads were harvested to measure the expression of GLUT4 mRNA by fluorescent quantitative RT-PCR and the GLUT4 protein level and insulin-stimulated transloeation were assessed by Western blot. Results Birth weight of FGR animals were significantly lower than that of control (t=6.399, P<0.01), but surpassed the control at 8 weeks with increased fasting IRI(P<0.05). The GLUT4 mRNA expression in adipose tissue of FGR rats (0.36± 0.04) was lower than that of control (1.01±0.11) (t=2.854, P<0.05). Declined total GLUT4 protein concentration(913.47±87.32) was also noted in the FGR group compared with the controls (1248.30± 131.52) (t=2.617, P<0.05). After administration of insulin, plasma membrane associated-GLUT4 concentration significantly increased to 897.03±102.87, which was equal to 2.12 times of the basal level (423.05±41.26) in control rats(t=4.759, P<0.01). However, insulin-responsive GLUT4 transloeation was markedly blunted in FGR rats(525.12±54.96) compared with controls, only increased to 1.38 times of the basal level (379.57±38.71)(t=2.083, P<0.05). Conclusions Decreased GLUT4 expression and insulin-stimulated translocation in adipose tissue of the male FGR offspring might be caused by exposure to protein malnutrition during pregnancy, which may disturb the uptake and utilization of glucose and subsequently be related to diabetes mellitus in later life.     

妊娠合并糖尿病对子代婴幼儿期胰岛素敏感性的影响

目的 探讨妊娠合并糖尿病对子代婴幼儿期胰岛素敏感性的影响.方法 本研究为前瞻性队列研究,在2、4、6、8、10、12、18和24月龄测量糖尿病母亲的子代和非糖尿病母亲的子代的体重、身长,计算体重指数.在6、12和24月龄随访当日测定空腹血浆血糖和空腹血清胰岛素(fasting seruminsulin,FINS),计算胰岛素敏感指数(insulin sensitivityindex,ISI),采用胰岛素稳态模型(homeostasis model assessment,HOMA)计算胰岛素抵抗(insulin resistence,IR)指数,即HOMA-IR,将FINS、ISI和HOMA-IR作为胰岛素敏感性评价指标.采用协方差分析比较2组间胰岛素敏感性的差异.结果 最初纳入研究的婴幼儿共605例,其中糖尿病母亲的子代94例,非糖尿病母亲的子代511例.糖尿病母亲的子代在2、4和6月龄时体重、身长均大于非糖尿病母亲的子代,2和4月龄时体重指数也大于非糖尿病母亲的子代,差异均有统计学意义(P＜0.05).在6、12和24月龄测定空腹血浆血糖和FINS的婴幼儿分别有276例、273例和56例.糖尿病母亲的子代在6、12和24月龄时的FINS[经对数(Lg)转换]分别为0.95±0.30、0.89±0.34和0.90±0.27,HOMA-IR值[经对数(Lg)转换]分别为0.34±0.33、0.27士0.36和0.27±0.31,ISI[经对数(Ln)转换]分别为-3.87±0.75、-3.73±0.81和-3.73±0.71;FINS和HOMA-IR值高于非糖尿病母亲的子代(FINS分别为0.70±0.45、0.73±0.35和0.67±0.30,HOMA-IR分别为0.08±0.46、0.10±0.36和0.03±0.33),差异有统计学意义(t=9.58、5.01、6.11、9.55、4.79和5.06,P均＜0.05);ISI低于非糖尿病母亲的子代(分别为-3.29±1.05、-3.35±0.84和-3.18±0.77),差异有统计学意义(t=9.20、4.90和5.06,P均＜0.05).糖尿病母亲的子代胰岛素敏感者22例,其中母乳喂养9例(40.91%),混合喂养7例(31.82%),配方乳喂养6例(27.27%);胰岛素不敏感者72例,其中母乳喂养12例(16.67%),混合喂养21例(29.17%)、配方乳喂养39例(54.17%),差异有统计学意义(x2=7.02,P=0.03).结论 妊娠合并糖尿病对子代婴幼儿期的胰岛素敏感性有不良影响,并且影响婴儿早期的生长发育,而母乳喂养可能有助于减少婴幼儿期胰岛素抵抗.

Abstract：

Objective To investigate the effects of pregnancy complicated with diabetes on the insulin sensitivity of offspring during their early childhood. Methods Offspring of diabetic mothers(ODM) and of non-diabetic mothers(ONDM) aged 1 month to 24 months were recruited into this prospective cohort study and followed up for two years. Body weight and body length were measured at 2, 4, 6, 8, 10, 12, 18 and 24 months of age respectively, and body mass index (BMI) were calculated. Fasting plasma glucose and fasting serum insulin levels were measured on the following-up day at 6, 12 and 24 months of age and insulin sensitivity index (ISI) was calculated. Homeostasis model assessment was used to calculate the insulin resistance (HOMA-IR). Insulin sensitivity was evaluated by fasting serum insulin, ISI and HOMA-IR. The difference of insulin sensitivity between ODM and ONDM group were examined by analysis of covariance adjusted by gender, gestational age,birth weight and BMI. Results Six hundred and five babies including ninety ODM and five hundred and eleven ONDM met the inclusion criteria. There were no differences in gender, gestational age,birth-weight/height between the two groups(P＞0. 05). ODM were heavier and higher than ONDM at each measure point during early childhood, but there were statistical differences at the age of 2, 4 and 6 months only (P＜0. 05). And the BMI at age of 2 and 4 months of ODM were higher than those of ONDM(P＜0.05). The number of baby who accepted the measurement of fasting plasma glucose and fasting serum insulin levels at 6, 12 and 24 months of age was 276 cases, 273 cases and 56 cases respectively. The fasting serum insulin of ODM (logarithmically transformed) were 0. 95±0. 30,0. 89±0. 34 and 0. 90±0. 27, which were higher than those of ONDM (0. 70±0. 45, 0. 73±0. 35 and 0. 67±0. 30) (t=9. 58, 5.01 and 6. 11, P＜0.05); HOMA-IR (logarithmically transformed) were 0. 34±0. 33, 0. 27±0. 36 and 0. 27±0. 31, which were higher than those of ONDM also(0.08±0. 46,0. 10±0. 36 and 0. 03 ± 0.33) (t= 9. 55, 4. 79 and 5. 06, P＜0.05); ISI(natural logarithmically transformed) were -3.87±0. 75, -3.73±0. 81 and -3. 73±0. 71, which were lower than those of ONDM(-3.29±1.05, -3.35±0.84 and -3.18±0. 77) (t=9.20, 4. 90 and 5.06, P＜0.05).There were differences in feeding characteristics of ODM between insulin sensitive subgroup [40. 9%(9/22) breast-feeding] and insulin insensitive subgroup [16.67 % (12/72) breast-feeding] (x2 = 7.02,P=0. 03). Conclusions Pregnancy complicated with diabetes has adverse effects on the offspring insulin sensitivity during their early childhood, and affects the early growth and development of them.Breast-feeding might decrease insulin resistance in babies.     

妊娠期糖尿病母鼠血清晚期糖基化终产物与子鼠心脏发育异常的关系

Objective To explore the effect of advanced glycation end product(AGE) in serum of maternal rats with gestational diabetes mellitus (GDM) on the heart development of their offsprings. Methods Fifty-four SD rats were randomly assigned into control group (n= 24) and GDM group (n=30) which were established by administration of streptozotocin intra-abdominally. On the gestational age of 13, 16, 19 days, all rats underwent hysterectomy to obtain the fetal heart tissues. Serum level of AGE and blood glucose level of maternal rats were tested. The expression of receptor AGE (RAGE) in fetal cardiac tissue were detected by immunohistoehemistry. Results The incidence of fetal heart defect in GDM group was significantly higher than the control group at each time point (P<0.01). Rats in GDM group had higher blood glucose level at each time point (P<0.01). The AGE levels of GDM group on gestational age of 13, 16 and 19 day [(5.72±0.68) U/mgpr, (7.31±0.29) U/mgpr and (7.77±0.39) U/mgpr] were significantly higher than those of the control group [(4.45±0.27) U/mgpr, (4.71±0. 35) U/mgpr and (4. 37±0. 44) U/rngpr] (t=6. 142, 16. 295, 0. 399,P<0. 01). The number of heart malformation in fetal rats (r=0.994,P=0. 000) and blood glucose (r=0. 717,P=0. 000) had the positive relationship with the maternal serum AGE level. The expression of RAGE in fetal heart was positively related with the number of fetal heart malformation (r= 0. 638,P= 0. 004). Conclusions The increased maternal serum AGE level in GDM rats may be an important factor in fetal heart dysplasia.     

妊娠期糖尿病母鼠血清晚期糖基化终产物与子鼠心脏发育异常的关系

Objective To explore the effect of advanced glycation end product(AGE) in serum of maternal rats with gestational diabetes mellitus (GDM) on the heart development of their offsprings. Methods Fifty-four SD rats were randomly assigned into control group (n= 24) and GDM group (n=30) which were established by administration of streptozotocin intra-abdominally. On the gestational age of 13, 16, 19 days, all rats underwent hysterectomy to obtain the fetal heart tissues. Serum level of AGE and blood glucose level of maternal rats were tested. The expression of receptor AGE (RAGE) in fetal cardiac tissue were detected by immunohistoehemistry. Results The incidence of fetal heart defect in GDM group was significantly higher than the control group at each time point (P<0.01). Rats in GDM group had higher blood glucose level at each time point (P<0.01). The AGE levels of GDM group on gestational age of 13, 16 and 19 day [(5.72±0.68) U/mgpr, (7.31±0.29) U/mgpr and (7.77±0.39) U/mgpr] were significantly higher than those of the control group [(4.45±0.27) U/mgpr, (4.71±0. 35) U/mgpr and (4. 37±0. 44) U/rngpr] (t=6. 142, 16. 295, 0. 399,P<0. 01). The number of heart malformation in fetal rats (r=0.994,P=0. 000) and blood glucose (r=0. 717,P=0. 000) had the positive relationship with the maternal serum AGE level. The expression of RAGE in fetal heart was positively related with the number of fetal heart malformation (r= 0. 638,P= 0. 004). Conclusions The increased maternal serum AGE level in GDM rats may be an important factor in fetal heart dysplasia.     

妊娠期糖尿病母鼠血清晚期糖基化终产物与子鼠心脏发育异常的关系

Objective To explore the effect of advanced glycation end product(AGE) in serum of maternal rats with gestational diabetes mellitus (GDM) on the heart development of their offsprings. Methods Fifty-four SD rats were randomly assigned into control group (n= 24) and GDM group (n=30) which were established by administration of streptozotocin intra-abdominally. On the gestational age of 13, 16, 19 days, all rats underwent hysterectomy to obtain the fetal heart tissues. Serum level of AGE and blood glucose level of maternal rats were tested. The expression of receptor AGE (RAGE) in fetal cardiac tissue were detected by immunohistoehemistry. Results The incidence of fetal heart defect in GDM group was significantly higher than the control group at each time point (P<0.01). Rats in GDM group had higher blood glucose level at each time point (P<0.01). The AGE levels of GDM group on gestational age of 13, 16 and 19 day [(5.72±0.68) U/mgpr, (7.31±0.29) U/mgpr and (7.77±0.39) U/mgpr] were significantly higher than those of the control group [(4.45±0.27) U/mgpr, (4.71±0. 35) U/mgpr and (4. 37±0. 44) U/rngpr] (t=6. 142, 16. 295, 0. 399,P<0. 01). The number of heart malformation in fetal rats (r=0.994,P=0. 000) and blood glucose (r=0. 717,P=0. 000) had the positive relationship with the maternal serum AGE level. The expression of RAGE in fetal heart was positively related with the number of fetal heart malformation (r= 0. 638,P= 0. 004). Conclusions The increased maternal serum AGE level in GDM rats may be an important factor in fetal heart dysplasia.     

妊娠期糖尿病母鼠血清晚期糖基化终产物与子鼠心脏发育异常的关系

Objective To explore the effect of advanced glycation end product(AGE) in serum of maternal rats with gestational diabetes mellitus (GDM) on the heart development of their offsprings. Methods Fifty-four SD rats were randomly assigned into control group (n= 24) and GDM group (n=30) which were established by administration of streptozotocin intra-abdominally. On the gestational age of 13, 16, 19 days, all rats underwent hysterectomy to obtain the fetal heart tissues. Serum level of AGE and blood glucose level of maternal rats were tested. The expression of receptor AGE (RAGE) in fetal cardiac tissue were detected by immunohistoehemistry. Results The incidence of fetal heart defect in GDM group was significantly higher than the control group at each time point (P<0.01). Rats in GDM group had higher blood glucose level at each time point (P<0.01). The AGE levels of GDM group on gestational age of 13, 16 and 19 day [(5.72±0.68) U/mgpr, (7.31±0.29) U/mgpr and (7.77±0.39) U/mgpr] were significantly higher than those of the control group [(4.45±0.27) U/mgpr, (4.71±0. 35) U/mgpr and (4. 37±0. 44) U/rngpr] (t=6. 142, 16. 295, 0. 399,P<0. 01). The number of heart malformation in fetal rats (r=0.994,P=0. 000) and blood glucose (r=0. 717,P=0. 000) had the positive relationship with the maternal serum AGE level. The expression of RAGE in fetal heart was positively related with the number of fetal heart malformation (r= 0. 638,P= 0. 004). Conclusions The increased maternal serum AGE level in GDM rats may be an important factor in fetal heart dysplasia.     

妊娠期糖尿病母鼠血清晚期糖基化终产物与子鼠心脏发育异常的关系

Objective To explore the effect of advanced glycation end product(AGE) in serum of maternal rats with gestational diabetes mellitus (GDM) on the heart development of their offsprings. Methods Fifty-four SD rats were randomly assigned into control group (n= 24) and GDM group (n=30) which were established by administration of streptozotocin intra-abdominally. On the gestational age of 13, 16, 19 days, all rats underwent hysterectomy to obtain the fetal heart tissues. Serum level of AGE and blood glucose level of maternal rats were tested. The expression of receptor AGE (RAGE) in fetal cardiac tissue were detected by immunohistoehemistry. Results The incidence of fetal heart defect in GDM group was significantly higher than the control group at each time point (P<0.01). Rats in GDM group had higher blood glucose level at each time point (P<0.01). The AGE levels of GDM group on gestational age of 13, 16 and 19 day [(5.72±0.68) U/mgpr, (7.31±0.29) U/mgpr and (7.77±0.39) U/mgpr] were significantly higher than those of the control group [(4.45±0.27) U/mgpr, (4.71±0. 35) U/mgpr and (4. 37±0. 44) U/rngpr] (t=6. 142, 16. 295, 0. 399,P<0. 01). The number of heart malformation in fetal rats (r=0.994,P=0. 000) and blood glucose (r=0. 717,P=0. 000) had the positive relationship with the maternal serum AGE level. The expression of RAGE in fetal heart was positively related with the number of fetal heart malformation (r= 0. 638,P= 0. 004). Conclusions The increased maternal serum AGE level in GDM rats may be an important factor in fetal heart dysplasia.     

妊娠期糖尿病母鼠血清晚期糖基化终产物与子鼠心脏发育异常的关系

Objective To explore the effect of advanced glycation end product(AGE) in serum of maternal rats with gestational diabetes mellitus (GDM) on the heart development of their offsprings. Methods Fifty-four SD rats were randomly assigned into control group (n= 24) and GDM group (n=30) which were established by administration of streptozotocin intra-abdominally. On the gestational age of 13, 16, 19 days, all rats underwent hysterectomy to obtain the fetal heart tissues. Serum level of AGE and blood glucose level of maternal rats were tested. The expression of receptor AGE (RAGE) in fetal cardiac tissue were detected by immunohistoehemistry. Results The incidence of fetal heart defect in GDM group was significantly higher than the control group at each time point (P<0.01). Rats in GDM group had higher blood glucose level at each time point (P<0.01). The AGE levels of GDM group on gestational age of 13, 16 and 19 day [(5.72±0.68) U/mgpr, (7.31±0.29) U/mgpr and (7.77±0.39) U/mgpr] were significantly higher than those of the control group [(4.45±0.27) U/mgpr, (4.71±0. 35) U/mgpr and (4. 37±0. 44) U/rngpr] (t=6. 142, 16. 295, 0. 399,P<0. 01). The number of heart malformation in fetal rats (r=0.994,P=0. 000) and blood glucose (r=0. 717,P=0. 000) had the positive relationship with the maternal serum AGE level. The expression of RAGE in fetal heart was positively related with the number of fetal heart malformation (r= 0. 638,P= 0. 004). Conclusions The increased maternal serum AGE level in GDM rats may be an important factor in fetal heart dysplasia.     

妊娠期糖尿病母鼠血清晚期糖基化终产物与子鼠心脏发育异常的关系

Objective To explore the effect of advanced glycation end product(AGE) in serum of maternal rats with gestational diabetes mellitus (GDM) on the heart development of their offsprings. Methods Fifty-four SD rats were randomly assigned into control group (n= 24) and GDM group (n=30) which were established by administration of streptozotocin intra-abdominally. On the gestational age of 13, 16, 19 days, all rats underwent hysterectomy to obtain the fetal heart tissues. Serum level of AGE and blood glucose level of maternal rats were tested. The expression of receptor AGE (RAGE) in fetal cardiac tissue were detected by immunohistoehemistry. Results The incidence of fetal heart defect in GDM group was significantly higher than the control group at each time point (P<0.01). Rats in GDM group had higher blood glucose level at each time point (P<0.01). The AGE levels of GDM group on gestational age of 13, 16 and 19 day [(5.72±0.68) U/mgpr, (7.31±0.29) U/mgpr and (7.77±0.39) U/mgpr] were significantly higher than those of the control group [(4.45±0.27) U/mgpr, (4.71±0. 35) U/mgpr and (4. 37±0. 44) U/rngpr] (t=6. 142, 16. 295, 0. 399,P<0. 01). The number of heart malformation in fetal rats (r=0.994,P=0. 000) and blood glucose (r=0. 717,P=0. 000) had the positive relationship with the maternal serum AGE level. The expression of RAGE in fetal heart was positively related with the number of fetal heart malformation (r= 0. 638,P= 0. 004). Conclusions The increased maternal serum AGE level in GDM rats may be an important factor in fetal heart dysplasia.     

妊娠期糖尿病母鼠血清晚期糖基化终产物与子鼠心脏发育异常的关系

Objective To explore the effect of advanced glycation end product(AGE) in serum of maternal rats with gestational diabetes mellitus (GDM) on the heart development of their offsprings. Methods Fifty-four SD rats were randomly assigned into control group (n= 24) and GDM group (n=30) which were established by administration of streptozotocin intra-abdominally. On the gestational age of 13, 16, 19 days, all rats underwent hysterectomy to obtain the fetal heart tissues. Serum level of AGE and blood glucose level of maternal rats were tested. The expression of receptor AGE (RAGE) in fetal cardiac tissue were detected by immunohistoehemistry. Results The incidence of fetal heart defect in GDM group was significantly higher than the control group at each time point (P<0.01). Rats in GDM group had higher blood glucose level at each time point (P<0.01). The AGE levels of GDM group on gestational age of 13, 16 and 19 day [(5.72±0.68) U/mgpr, (7.31±0.29) U/mgpr and (7.77±0.39) U/mgpr] were significantly higher than those of the control group [(4.45±0.27) U/mgpr, (4.71±0. 35) U/mgpr and (4. 37±0. 44) U/rngpr] (t=6. 142, 16. 295, 0. 399,P<0. 01). The number of heart malformation in fetal rats (r=0.994,P=0. 000) and blood glucose (r=0. 717,P=0. 000) had the positive relationship with the maternal serum AGE level. The expression of RAGE in fetal heart was positively related with the number of fetal heart malformation (r= 0. 638,P= 0. 004). Conclusions The increased maternal serum AGE level in GDM rats may be an important factor in fetal heart dysplasia.     

宫内重度高血糖及出生后早期过度喂养与子鼠成年期代谢综合征

目的 探讨孕期重度高血糖及出生后早期过度喂养与子鼠成年期代谢表型的关系.方法 成年Wistar雌性大鼠于妊娠第5天腹腔内注射20%链脲霉素50 mg/kg,血糖＞20 mmol/L为孕期重度高血糖模型(severely diabetes mellitus,SDM).子鼠生后通过减少哺乳期胎仔数建立子鼠早期过度喂养模型.根据孕期血糖水平和哺乳期喂养方式将子鼠分为3组:(1)对照组子鼠(control pups,CP组):孕期母鼠血糖正常,哺乳期1只母鼠喂养8只子鼠;(2)SDM正常喂养组:孕期母鼠重度高血糖,哺乳期1只母鼠喂养8只子鼠;(3)SDM过度喂养组:孕期母鼠重度高血糖,哺乳期1只母鼠喂养4只子鼠.各组子鼠于第3周断乳后均给予常规饲料喂养.观察3～26周各组子鼠体重变化,测定26周龄时子鼠收缩压、舒张压、心率以及代谢相关指标,包括空腹总甘油三酯,总胆固醇、低密度脂蛋白胆固醇、高密度脂蛋白胆固醇,根据空腹血糖、空腹胰岛素水平利用胰岛素稳态模型(homeostasis model assessment,HOMA)计算胰岛素抵抗指数(insulin resistance,IR).组间各指标比较采用ANOVA和LSD检验.结果 SDM组母鼠空腹血糖为(28.34±5.14)mmol/L,明显高于对照组(6.25±1.41)mmol/L(P＜0.05).SDM过度喂养组和正常喂养组子鼠3周断乳后体重显著低于CP组[(43.63±4.83)g、(31.45±10.21)g和(55.75±8.4)g,P＜0.05],SDM过度喂养组 3～6周体重均明显高于SDM正常喂养组(P＜0.05).SDM组子鼠3～7周、3～9周体重增长率高于CP组,其中SDM正常喂养组与SDM过度喂养组和CP组间差异均有统计学意义(P＜0.05).生后26周龄时SDM正常喂养组和SDM过度喂养组收缩压[(153.31±13.91)mm Hg和(147.21±12.29)mm Hg]和甘油三酯[(0.73±0.22)mmol/L和(0.71±0.49)mmol/L]水平明显高于CP组[分别为(132.21±11.26)mm Hg和(0.37±0.08)mmol/L](P均＜0.05),但SDM正常喂养组和SDM过度喂养组之间差异无统计学意义(P＞0.05).SDM正常喂养组、SDM过度喂养组和CP组间空腹血糖水平差异无统计学意义,但SDM过度喂养组的空腹胰岛素和HOMA-IR分别为(12.552±3.260)mU/L和2.400±0.624,与SDM正常喂养组[分别为(9.067±1.782)mU/L和1.797±0.508]和CP组[分别为(8.590±0.806)mU/L和1.729±0.246]比较,显著增高(P＜0.05).结论 孕期重度高血糖可导致子鼠低出生体重,生后早期存在明显的追赶生长.子鼠成年期代谢综合征的发病风险增加,早期过度喂养可加速这一进程.     

血糖控制满意的妊娠期糖尿病孕妇血清性激素结合球蛋白水平与妊娠结局的关系

目的 探讨血糖控制满意的妊娠期糖尿病(GDM)孕妇血清性激素结合球蛋白(SHBG)水平与妊娠结局的关系.方法 选择2005年3月至2010年3月在中国医科大学附属盛京医院产科门诊确诊的妊娠24～28周GDM孕妇251例,其中经单纯饮食控制(169例)或加用胰岛素治疗(47例)后血糖控制满意的216例为血糖控制满意组;经单纯饮食控制或加用胰岛素治疗后血糖控制不满意的35例为血糖控制不满意组.选取同期妊娠24～28周的192例健康孕妇为健康对照组.分别于妊娠24～28周和妊娠＞36周两次测定孕妇血清SHBG水平和稳态模型的胰岛素抵抗(HOMA-IR)指数.依据美国糖尿病资料小组的GDM诊断标准采用"两步法"诊断GDM.记录并观察3组孕妇的妊娠结局.测定孕妇空腹血糖(FPG)和空腹胰岛素(FINS)水平.结果 (1)妊娠结局比较:血糖控制满意组孕妇的妊娠期高血压疾病(10.6%,23/216)、早产(8.3%,18/216)、大于胎龄儿(8.8%,19/216)、新生儿窒息(3.7%,8/216)和新生儿低血糖(2.3%,5/216)的发生率明显低于血糖控制不满意组[分别为42.9%(15/35)、34.3%(12/35)、31.4%(11/35)、22.9%(8/35)和11.4%(4/35)],两组分别比较,差异均有统计学意义(P＜0.05或P＜0.01);而两组孕妇羊水过多、产褥感染、产后出血和新生儿高胆红素血症的发生率比较,差异均无统计学意义(P＞0.05).血糖控制满意组孕妇早产、产褥感染(3.2%,7/216)、产后出血(5.1%,11/216)、新生儿窒息(3.7%,8/216)和新生儿低血糖(2.3%,5/216)的发生率,与健康对照组[分别为7.3%(14/192)、2.1%(4/192)、4.2%(8/192)、2.1%(4/192)和1.6%(3/192)]比较,差异均无统计学意义(P＞0.05).(2)妊娠24～28周与妊娠＞36周孕妇血清SHBG等项指标检测结果比较:血糖控制满意组孕妇血清SHBG水平[分别为(384±88)及(457±48)nmo]/L]均明显高于血糖控制不满意组[分别为(313±45)及(401±73)nmol/L];血糖控制满意组孕妇HOMA-IR指数(分别为5.3±1.1及5.5±1.1)均明显低于血糖控制不满意组(分别为7.0±1.3及7.6±1.7),两组分别比较,差异均有统计学意义(P＜0.01);血糖控制满意组孕妇血清SHBG水平均明显低于健康对照组[分别为(492±95)及(565±40)nmol/L];而HOMA-IR指数均明显高于健康对照组(分别为3.6±0.6及3.9±0.5),两组分别比较,差异均有统计学意义(P＜0.01);血糖控制满意组孕妇FPG水平[分别为(5.84±0.28)及(5.16±0.13)mmol/L]明显低于血糖控制不满意组[分别为(6.13±0.16)及(5.68±1.14)mmol/L],两组分别比较,差异均有统计学意义(P＜0.01);血糖控制满意组孕妇FINS水平[分别为(20.4±2.1)及(24.1±4.2)mmol/L]明显低于血糖控制不满意组[分别为(24.7±4.5)及(29.9±2.7)mmol/L],两组分别比较,差异均有统计学意义(P＜0.01).(3)相关性分析:妊娠24～28周时,3组孕妇(共443例)血清SHBG水平与HOMA-IR指数呈负相关(r=-0.952,P＜0.01);其中血糖控制满意组216例孕妇血清SHBG水平与HOMA-IR指数也呈负相关(r=-0.903,P＜0.01).结论 血糖控制满意的GDM孕妇并不能完全改善妊娠结局,GDM孕妇血清SHBG水平降低和高IR对其妊娠结局有一定影响.

Abstract：

Objective To explore the relationship between sex hormone-binding globulin (SHBG) of gestational diabetes mellitus ( GDM ) pregnant women with well-controlled glucose and pregnancy outcomes. Methods Two hundred and fifty-one GDM pregnant women of 24 - 28 weeks in Shengjing Hospital of China Medical University were recruited from Mar. 2005 to Mar. 2010. Two hundred and sixteen cases of GDM with well-controlled glucose were defined as glycemic satisfied group, and they were treated by diet therapy ( 169 cases) or insulin therapy (47 cases) . Thirty-five cases with unsatisfied glucose were defined as glycemic unsatisfied group. One hundred and ninety-two healthy pregnant women of 24 - 28 weeks were defined as healthy control group. Serum SHBG and homeostasis model analysis of insulin resistance ( HOMA-IR) at 24 - 28 weeks and above 36 weeks were measured. GDM was diagnosed by " two-step" method according to the National Diabetes Data Group ( NDDG) criteria. The pregnancy outcomes and complications of the three groups were recorded. Results ( 1 ) Comparison of pregnancy outcomes and complications: glycemic satisfied group was less likely to develop hypertensive disorders in pregnancy ( 10. 6% ) , premature birth(8. 3% ) ,large for gestational age ( LGA) (8. 8% ) , neonatal asphyxia(3. 7% ) and neonatal hypoglycemia ( 2. 3% ) compared to glycemic unsatisfied group ( 42. 9% , 34. 3% , 31. 4% , 22. 9% and 11. 4% ,respectively). And the difference was statistically significant (P ＜0. 05 or P ＜0. 01). There was no significant difference for incidence of polyhydramnios, pueperal infection, postpartum hemorrhage, neonatal hyperbilirubinemia between the two groups ( P＞ 0. 05 ) . When compared to healthy control group(7. 3% ,2. 1% ,4. 2% ,2. 1% and 1. 6% ) ,no significant difference was found for incidence of premature birth( 8. 3% ) , pueperal infection ( 3. 2% ) , postpartum hemorrhage (5. 1% ) , neonatal asphyxia (3. 7% )and neonatal hypoglycemia(2. 3% ,P ＞0. 05). (2) Comparison of results of 24 - 28 weeks and above 36 weeks: serum SHBG of glycemic satisfied group [( 384 ± 88 ) , (457 ± 48 ) nmol/L]was significantly higher than that of glycemic unsatisfied group[(313 ±45) ,(401 ±73) nmol/L];HOMA-IR of glycemic satisfied group (5. 3 ±1.1,5.5 ±1.1) was significantly lower than that of glycemic unsatisfied group (7. 0 ± 1. 3 ,7. 6 ± 1. 7 ; P ＜ 0. 01). Serum SHBG of glycemic satisfied group was significantly lower than that of healthy control group [( 492 ± 95 ) , (565 ± 40 ) nmol/L]; and HOMA-IR of glycemic satisfied group(5. 3 ± 1. 1,5. 5 ± 1. 1) was significantly higher than that of healthy control group (3. 6 ±0. 6,3. 9 ± 0. 5 ;P ＜ 0. 01 ) . FPG of glycemic satisfied group [( 5. 84 ± 0. 28 ) , ( 5. 16 ± 0. 13 ) mmol/L]was significantly lower than that of glycemic unsatisfied group [(6. 13 ± 0. 16 ) , ( 5. 68 ± 1. 14) mmol/L; P ＜ 0. 01]. FINS of glycemic satisfied group [( 20. 4 ± 2. 1 ) , ( 24. 1 ± 4. 2 ) mmol/L]was significantly lower than that of glycemic unsatisfied group [(24. 7 ± 4. 5 ) , ( 29. 9 ± 2. 7 ) mmol/L; P ＜ 0. 01]. ( 3 ) Correlation analysis. Between 24 - 28 weeks, SHBG was negatively correlated with HOMA-IR in the three groups ( r = -0. 952, P ＜0. 01) ; and SHBG was negatively correlated with HOMA-IR in glycemic satisfied group ( r = -0. 903, P ＜0. 01). Conclusions Well-controlled glucose can not completely improve maternal and fetal outcomes of GDM pregnant women. High insulin resistance and low serum SHBG can influence pregnancy outcomes.     

子宫内高糖环境与子代成年期瘦素抵抗的动物实验研究

目的 探讨宫内暴露于高糖环境下的仔鼠成年期瘦素水平的变化以及对其生长发育的影响.方法 采用成年Wistar雌鼠与Wistar雄鼠杂交,在孕鼠妊娠第5天给予20%链脲霉素50 mg/kg腹腔内注射,建立高糖环境模型,为高糖组;孕鼠腹腔内仅注射柠檬酸缓冲液作为对照组.测量两组仔鼠3～10周龄的体重增长;仔鼠11周龄时,采用酶联免疫吸附试验检测其血浆瘦素水平,分析瘦素与仔鼠生长发育的相关性;应用免疫组化方法及实时定量PCR技术分别检测仔鼠下丘脑瘦素受体蛋白及mRNA表达水平[以积分吸光度(IA)值表示].结果 (1)高糖组母鼠空腹血糖为(28.3±5.1)mmol/L,明显高于对照组的(6.3±1.4)mmol/L,两组比较,差异有统计学意义(P＜0.05).仔鼠11周龄时,高糖组仔鼠空腹血糖为(5.1±0.8)mmol/L,对照组仔鼠空腹血糖为(5.3±0.6)mmol/L,两组比较,差异无统计学意义(P＞0.05).(2)高糖组仔鼠出生后3～10周的体重增长率为649.7%,显著高于对照组的479.2%,两组比较,差异有统计学意义(P＜0.05).(3)高糖组仔鼠基础胰岛素水平为(0.76±0.37)μg/,L,对照组仔鼠为(1.06±0.14)μg/L,两组比较,差异有统计学意义(P＜0.05);高糖组仔鼠基础瘦素水平为(113±37)μg/L,对照组仔鼠为(128±40)μg/L,两组比较,差异无统计学意义(P＞0.05).(4)高糖组仔鼠瘦素水平与体重增长率无相关性(r=-0.501,P=0.311);对照组仔鼠瘦素水平与体重增长率有显著负相关关系(r=-0.553,P=0.001).(5)高糖组仔鼠11周龄时下丘脑瘦素受体蛋白表达水平为4125±414,对照组仔鼠11周龄时下丘脑瘦素受体蛋白表达水平为4244±511,两组比较,差异无统计学意义(P＞0.05).高糖组仔鼠11周龄时下丘脑瘦素受体mRNA表达水平中位数为1.25,对照组仔鼠11周龄时下丘脑瘦素受体mRNA表达水平中位数为1.80,高糖组虽低于对照组,但差异无统计学意义(P＞0.05).结论 大鼠宫内高糖环境会导致仔鼠出生后3～10周体重过快增长,而瘦素水平无下降趋势,提示可能存在一定程度的瘦素抵抗;但未影响仔鼠出生后11周时的下丘脑瘦素受体表达水平的变化,宫内暴露于高糖环境下仔鼠发生的成年期瘦索抵抗并非通过下丘脑瘦素受体水平的变化所导致.     

复方当归注射液可减轻大剂量柴油机尾气颗粒物对雌性小鼠卵和卵裂球的损伤

目的 观察雌性小鼠亚急性接触柴油机尾气颗粒物(diesel exhaust particles,DEP)致卵和卵裂球损伤以及复方当归注射液对损伤的干预效果.方法 210只21 d ICR雌鼠随机分为对照组(A组)、DEP组(B组)、DEP+小剂量组(C组)、DEP+中剂量组(D组)和DEP+大剂量组(E组)(各42只),分别向小鼠咽后壁接种12.0 μg/μl DEP混悬液(B～E组)或载液(PBS,A组)各30μl,每3 d重复接种1次,共4次.末次DEP接触后3 d处死动物.C、D、E组首次接种日至处死前1 d,每日分别经腹腔给予复方当归注射液相当于生药75、150和300 mg各1次,连续给药12次.观察指标包括小鼠一般情况、体重;卵巢重量、卵巢重量/体重比值、卵巢组织超氧化物歧化酶(superoxide dismutase,SOD)活性、还原型谷胱甘肽(reduced glutathione,GSH)和丙二醛(malonaldehyde,MDA)含量;卵母细胞的存活率、胚泡破裂比率、第一极体释放率、受精率、线粒体DNA含量和超微结构变化.结果 (1)各组小鼠体重差异无统计学意义(P＞0.05).卵巢重量、卵巢重量/体重比值、卵巢SOD活性和GSH含量B组分别为(1.5±0.6)mg、(7.2±2.5)×10-5、(192.10±23.67)nU/mg prot和(262.40±31.60)nmol/mg prot,C组分别为(1.7±0.2)mg、(8.9±0.6)×10-5、(198.92±24.27)nU/rng prot和(271.66±14.58)nmol/mg prot,D组分别为(2.1±0.2)mg、(9.8±1.1)×10-5、(214.37±27.19)nU/mg prot和(285.93±9.55)nmol/mg prot,低于A组,分别为(3.3±1.5)mg、(15.4±7.3)×10-5、(292.30±40.03)nU/mg prot和(367.98±24.59)nmol/mg prot(P＜0.05或＜0.01);E组分别为(3.7±1.1)mg、(18.7±5.4)×10-5、(279.10±12.63)nU/mg prot和(353.59±10.61)nmol/mg prot,显著高于B组(P＜0.01);MDA含量B、C、D组分别为(3.88±0.35)nmol/mg prot、(3.62±0.19)nmol/mg prot和(2.63±0.34)nmol/mg prot,显著高于A组的(2.18±0.44)nmol/mg prot(P＜0.05或＜0.01),D、E组[(2.35±0.37 nmol/mg prot]显著低于B组(P＜0.01).(2)观察时间B、C组卵母细胞存活率以及B、C、D组第一极体释放率和24 h体外受精率显著低于A组(P＜0.05或P＜0.01),E组显著高于B组(P＜0.05);各组胚泡破裂比率均为100%.(3)卵母细胞线粒体DNA的拷贝数对数值,与A组比较,C、D、E组显著降低(P＜0.01);与B组比较,C、D组显著降低而E组显著升高(P＜0.01).(4)A组卵母细胞结构无明显改变;B、C组卵母细胞许多细胞器退变明显,部分细胞坏死;D组细胞内较多线粒体肿胀、空泡化,E组这些变化范围及程度均减小.结论复方当归注射液对雌性小鼠亚急性接触DEP所致的卵和卵裂球损害有治疗及保护作用.     

胎儿生长受限仔鼠脂肪组织中葡萄糖转运蛋白4的表达和细胞转位变化

目的 探讨胎儿生长受限(FGR)仔鼠脂肪组织中葡萄糖转运蛋白4(GLUT4)的表达和转位变化及其与胰岛素抵抗的关系. 方法 采用妊娠期全程低蛋白饮食法建立大鼠FGR模型,并设立对照组.观察雄性仔鼠生后体重增长和胰岛素抵抗指数(IRI)变化,采用荧光定量逆转录聚合酶链反应技术检测脂肪组织中GLUT4 mRNA表达,Western印迹法检测基础状态下脂肪组织中GLUT4的蛋白表达,以及胰岛素刺激后GLUT4向细胞膜的转位变化. 结果 (1)FGR组仔鼠平均出生体重明显低于对照组(t=6.399,P<0.01),8周龄时体重超过对照组,且空腹IRI增高(P均<0.05).(2)基础状态下,FGR组脂肪组织中GLUT4的mRNA表达(0.36±0.04)明显低于对照组(1.01±0.11)(t=2.854,P<0.05),GLUT4总蛋白含量(913.47±87.32)也低于对照组(1248.30±131.52)(t=2.617,P<0.05).胰岛素刺激后,对照组细胞膜中GLUT4蛋白浓度显著升高(897.03±102.87),是基础状态(423.05±41.26)的2.12倍(t=4.759,P<0.01),而FGR组对外源性胰岛素反应迟钝,细胞膜中GLUT4蛋白含量(525.12±54.96)仅是基础状态(379.57±38.71)的1.38倍(t=2.083,P<0.05). 结论 宫内蛋白质营养不良导致子代脂肪组织GLUT4蛋白表达降低和胰岛素介导的转位受阻,可能与葡萄糖摄取和利用障碍,促进糖尿病发生有关.     

生命早期的免疫应激对雌鼠青春期生殖功能的影响

目的 研究生命早期的免疫应激对雌鼠青春期生殖功能的影响.方法 雌性Sprague-Dawley大鼠在出生后第3、5天行腹腔注射脂多糖(50 μg/kg)和生理盐水作为实验组和对照组.每周测体质量,生后30 d开始监测青春期启动(即阴道口初开放)时间和卵巢周期的变化.生后6周行卵巢切除术,观察卵巢组织形态学的变化(卵泡内膜厚度和各种类型卵泡的数目);用免疫组化方法测定卵巢交感神经兴奋性的改变[以低亲和力的神经生长因子受体(p75NGFR)的免疫染色强度表示].结果 生命早期的免疫应激(暴露于脂多糖),能延迟阴道口初开放的时间,实验组大鼠为生后(40.6±0.7)d,对照组为生后(38.6±0.6)d,两组比较,差异有统计学意义(P＜0.05);降低卵巢正常周期的比例,实验组为26.1%,对照组为66.8%,两组比较,差异有统计学意义(P＜0.05);减少各种类型卵泡的数目,实验组大鼠原始卵泡(610±47)个、初级卵泡(624±41)个、窦前卵泡(183±16)个、窦卵泡(32±4)个,对照组分别为(1181±57)、(960±30)、(260±14)、(79±7)个,分别比较,差异均有统计学意义(P＜0.05);增加卵泡内膜厚度,实验组及对照组分别为(15.8±0.4)、(11.4±0.3)μm,两组比较,差异有统计学意义(P＜0.05).实验组大鼠的卵巢p75NGFR免疫染色强度较对照组明显增高(P＜0.05).结论 雌鼠生命早期的免疫应激对其青春期的生殖功能有明显的影响.生命早期的免疫应激可能通过上调卵巢交感神经兴奋性而推迟青春期发育,并减少卵巢正常周期的比例和卵泡储备,使卵泡内膜增厚.

Abstract：

Objective To investigate the long-term programming effects on pubertal reproductive function by immunological challenge in early life. Methods Female Sprague-Dawley rats were administered by endotoxin (lipopolysaccharide, LPS) at a dosage of 50 μg/kg and saline intraperitoneally on postnatal day 3 and 5. Body weight was measured weekly. Puberty onset ( vaginal opening) and oestrous cyclicity were monitored from postnatal day 30. At the age of 6 weeks, bilateral ovariectomy was performed. The histological and morphological change of the ovaries (the thickness of the theca interna and the number of different kinds of follicles) were observed and the immunoreactivity of the ovarian sympathetic nerve markers (low affinity receptor of nerve growth factor, p75NGFR) was evaluated by immune staining. Results Immunological challenge (exposed to LPS) in early life delayed vaginal opening significantly [LPS-treated (40.6 ±0.7) days versus controls ( 38. 6 ± 0. 5 ) days, P ＜ 0. 05], decreased the percentage of normal oestrous cyclicity ( LPS-treated 26. 1% versus controls 66. 8% , P＜ 0. 05 ) , decreased the total number of different types of follicles (primordial follicles: LPS-treated 610 ±47 versus controls 1181 ±57, P ＜ 0. 05; primary follicles: LPS-treated 624 ±41 versus controls 960 ± 30, P ＜ 0. 05 ; preantral follicles: LPS-treated 183 ± 16 versus controls 260 ± 14, P ＜ 0. 05; antral follicles: LPS-treated 32 ± 4 versus controls 79 ± 7, P ＜ 0. 05) and increased the thickness of the theca interna [LPS-treated ( 15. 8 ±0. 4) μm versus controls (11.4 ±0. 3) μm, P ＜ 0. 05]. The immunostaining of p75NGFR was obviously enhanced in the LPS-treated ovaries when compared with that of controls ( P ＜ 0. 05 ) . Conclusions Immunological stress during early critical developmental windows could have long dysfunctional effects on the pubertal reproductive function. It delayed puberty onset, reduced the percentage of the normal oestrous cycles, decreased follicles reserve and increased the thickness of the theca interna which might involve the up-regulation of the local ovarian sympathetic nerve activity.     

不同胎龄新生儿血清雌二醇水平变化及其与早产儿视网膜病的关系

目的 测定不同胎龄新生儿和早产儿视网膜病(retinopathy of prematurity,ROP)患儿血清雌二醇水平变化,探讨其与ROP发生发展的关系.方法 新人院新生儿184例.根据出生胎龄分为＜32周早产儿组、32～37周早产儿组和足月儿组,再根据是否吸氧分为未吸氧和吸氧两个亚 组.出生体重＜2000 g的早产儿均定期眼科筛查,确诊为ROP的患儿作为ROP组.各组分别在生 后第1、3、5、7周用放射免疫法检测血清雌二醇水平.组间结果比较采用非配对t检验和单因素方差 分析.结果 新生儿血清雌二醇水平随着日龄增加迅速下降.在未吸氧新生儿中,32～37周早产 儿组血清雌二醇水平在第1周和第3周分别为(3506±1376)pmol/L和(1431±92)pmol/L,显著高 于足月儿组[分别为(1717±179)pmol/L和(996±102)pmol/L](P均＜0.05);＜32周早产儿组仅第l周[(3173±1369) pmol/L]显著高于足月儿组(P＜0.05).＜32周早产儿血清雌二醇水平在生 后第5周为(560±355)pmol/L,明显低于32～37周早产儿[(1124±128)pmol/L](P＜0.05).在同一胎龄组中,吸氧与未吸氧患儿雌二醇水平差异均无统计学意义.ROP组与＜32周早产儿组血清雌 二醇水平差异无统计学意义.ROP组血清雌二醇水平在纠正胎龄29周和32～36周时低于非ROP 早产儿组,但差异无统计学意义.结论 早产儿低血清雌二醇水平可能与ROP发生有关.     

宫内窘迫胎儿出生后心肌损伤情况的监测

目的 探讨无窒息的宫内窘迫胎儿出生后是否合并有心肌损伤,以及检测心肌损伤的生化敏感指标.方法 2009年7月至12月,随机选择中山大学附属第一医院分娩的、有宫内窘迫史的53例新生儿为宫内窘迫组,新生儿出生后Apgar评分1 min及5 min均＞7分.同期分娩的无宫内窘迫史的新生儿36例作为对照组,新生儿出生后Apgar评分1 min及5 min均为10分.胎儿娩出后立即抽取脐动脉血进行血气分析和生化指标测定.结果 (1)宫内窘迫组新生儿脐动脉血pH值及剩余碱分别为7.23±0.07及(-4.8±3.0)mmol/L,明显低于对照组的7.31±0.03及(-2.1±1.5)mmol/L,两组比较,差异有统计学意义(P＜0.05).宫内窘迫组新生儿脐动脉血乳酸水平为(5.2±2.3)mmol/L,明显高于对照组的(2.3±1.1)mmol/L,两组比较,差异有统计学意义(P＜0.01).宫内窘迫组新生儿脐动脉血氧分压及二氧化碳分压水平分别为(16.2±7.9)及(54.0±11.2)mm Hg(1mm Hg=0.133 kPa),对照组分别为(17.5±6.7)及(48.5±5.4)mm Hg,两组分别比较,差异均无统计学意义(P＞0.05).(2)宫内窘迫组新生儿脐动脉血肌酸激酶同工酶MB(CK-MB)水平为(48±59)U/L,对照组为(36±27)U/L,两组比较,差异有统计学意义(P＜0.05);宫内窘迫组新生儿脐动脉血肌酸激酶(CK)及脑钠肽(BNP)水平分别为(194±73)U/L及(519±309)ng/L,对照组分别为(162±95)及(481±216)ng/L,两组比较,差异无统计学意义(P＞0.05).(3)新生儿脐动脉血CKMB水平与脐动脉血pH值、剩余碱呈负相关性(r=-0.296及-0.318,P均＜0.05);BNP与乳酸水平呈正相关(r=0.278,P＜0.05);其余各变量间均无相关性(P＞0.05).结论 宫内窘迫的胎儿即使出生时无新生儿窒息的表现,也存在着不同程度的心肌损伤;脐血CK-MB水平变化可作为监测心肌损伤的敏感指标,心肌损伤的程度与胎儿酸中毒的程度有关.

Abstract：

Objective To investigate whether no asphyxia neonates with intrauterine distress are complicated with myocardial injury and determine the sensitive biochemical diagnostic parameters. Methods A total of 89 neonates born in the First Affiliated Hospital of Sun Yat-sen University from July 2009 to December 2009 were enrolled. Fifty-three fetal distress cases with Apgar score ＞ 7 at 1 and 5 minites were enrolled in the study group; while the rest 36 healthy neonates, whose Apgar score = 10 at 1 and 5 minites, were the control group. Umbilical artery blood samples of all cases were collected for blood gas analysis and biochemical measurement. Results(1)pH(7.23±0.07) and BE [(-4.8±3.0)mmol/L] in the study group were significantly lower than pH (7.31 ±0.03) and BE [(-2.1±1.5)mmol/L] in the control group (P＜0.05).The lactic acid of study group [(5.2±2.3)mmol/L] was higher than that of the control group [(2.3±1.1)mmol/L], and the difference was significant (P＜0.01). However, there was no significant difference between the two groups in PaO2[(16.2±7.9)mm Hg(1 mm Hg=0.133 kPa) vs. (17.5±6.7)mm Hg] and PaCO2[(54.0±11.2)mm Hg vs. (48.5±5.4) mm Hg; P＞0. 05]. (2) The level of CK-MB in neonates with fetal distress[(48 ±59) U/L] was significantly higher than that of healthy neonates [(36±27)U/L]. However, no significant difference was found in CK [(194±73)U/L vs. (162±95) U/L]and BNP levels[(519±309)ng/L vs.(481±216)ng/L;P ＞ 0.05]. (3) Spearman rank correlation analysis showed that CK-MB level was negatively correlated with pH(r=-0.296, P＜0.05) and BE (r=-0.318,P＜0.05) of umbilical artery blood,while BNP level was positively correlated with umbilical lactic acid (r=0.278, P＜0.05). No correlation was found between other parameters (P＞0.05).Conclusions Intrauterine distress without neonatal asphyxia had effect on fetal myocardial injury. CK-MB can be used as a sensitive parameter for monitoring the development of myocardial injury. The severity of myocardial injury was related to fetal acidosis.