妊娠期合并糖代谢异常对新生儿胰岛素敏感性的影响

目的探讨妊娠期合并糖代谢异常对子代新生儿期胰岛素敏感性的影响。方法选择2009年12月至2010年11月本院产科出生的新生儿,根据母亲妊娠期是否合并糖代谢异常分为糖代谢异常母亲的新生儿和糖代谢正常母亲的新生儿。所有研究对象均进行出生体格测量,并于生后 3 天内测定空腹血糖( FPG) 和空腹血清胰岛素( FINS) ,计算胰岛素敏感指数( ISI) ,采用胰岛素稳态模型( HOMA) 计算胰岛素抵抗指数( IR) ,即 HOMA-IR,其中 FINS、ISI 和 HOMA-IR 值为胰岛素敏感性的评价指标。以性别、胎龄、出生体重为协变量,分别在早产儿和足月儿中进行胰岛素敏感性的协方差分析。结果 89 例早产新生儿和 96 例足月新生儿纳入分析。糖代谢异常母亲新生儿的出生体重、出生身长和重量指数( PI) 与糖代谢正常母亲的新生儿相比,差异无统计学意义( P >0. 05) 。与糖代谢正常母亲的早产儿相比,糖代谢异常母亲的早产儿 FPG 降低、FINS 升高,差异有统计学意义[FPG( mmol/L) : ( 4. 00 ±0. 25) 比( 4. 82 ±0. 18) ,FINS( 经对数 Lg 转换) : ( 0. 69± 0. 06) 比( 0. 54 ± 0. 04) ,P < 0. 05],ISI 值降低、HOMA-IR 值升高,但差异无统计学意义[ISI( 经对数 Ln 转换) : ( -2. 89 ±0. 15) 比( -2. 78 ±0. 11) ,HOMA-IR 值( 经对数 Lg 转换) : ( -0. 10 ±0. 06)比( -0. 15 ±0. 05) ,P >0. 05]; 足月儿中糖代谢异常母亲的新生儿 FPG、FINS 和 HOMA-IR 值低,ISI 值高,但差异均无统计学意义[FPG( mmol / L) : ( 4. 68 ± 0. 23) 比( 5. 17 ± 0. 13) ,FINS( 经对数 Lg转换) : ( 0. 56 ±0. 06) 比( 0. 61 ±0. 03) ,HOMA-IR 值( 经对数 Lg 转换) : ( -0. 14 ±0. 06) 比( -0. 03± 0. 03) ,ISI( 经对数 Ln 转换) : ( - 2. 79 ± 0. 14) 比( - 3. 04 ± 0. 08) ,P > 0. 05]。结论母亲妊娠期合并糖代谢异常虽然对新生儿的出生体重没有影响,但血糖仍然呈现低水平趋势,且对早产儿胰岛素敏感性可能有一定的影响。     

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.     

生长激素和胰岛素与新生儿宫内生长发育的关系

目的 探讨生长激素(GH)和胰岛素(INS)与新生儿宫内生长发育的关系.方法 研究对象为2010年1月-2011年1月在北京大学第三医院住院的73例健康足月新生儿和97例早产儿,研究对象均在出生24 h内取静脉血,采用酶联免疫吸附法检测血清GH和INS水平,同时核对胎龄及测量新生儿的出生体质量、头围和身长,比较新生儿出生24 h内血清GH和INS水平与胎龄、出生体质量、身长、头围的关系.结果 1.新生儿的胎龄与出生时血清GH水平呈负相关(r=-0.403,P=0.000),而与血清INS水平呈正相关(r=0.247,P=0.001);早产组出生时血清GH水平[(40.54±19.58) μg·L-1]显著高于足月组[(26.23±18.30) μg·L-1],而血清INS水平[(2.58±2.78) IU·L-1]则显著低于足月组[(4.02±3.60) IU·L-1](P=0.000,0.029).2.足月儿的出生体质量、身长、头围与出生时血清GH水平均呈负相关,而与血清INS水平均呈正相关;早产儿仅出生体质量与血清GH水平呈负相关,与血清INS水平呈正相关.3.足月新生儿出生时血清GH与INS水平无相关性(r=0.291,P= 0.090),而早产儿出生时血清GH与INS水平呈负相关(r=-0.353,P=0.004).结论 新生儿出生时GH和INS水平与其宫内发育密切相关,GH和INS可能参与调节新生儿宫内的生长发育.     

肝脏过氧化物体增殖物激活受体γ基因启动子甲基化及其mRNA表达下调降低胎儿生长受限大鼠胰岛素敏感性

目的 探讨肝脏过氧化物体增殖物激活受体γ (peroxisome proliferator-ativated receptorγ,PPARγ)基因启动子甲基化状态及其mRNA表达在胎儿生长受限(fetal growth restriction,FGR)大鼠胰岛素敏感性降低中的作用. 方法 20只雌鼠受孕后第1天随机分为对照组和低蛋白组,各10只.低蛋白组采用低蛋白(粗蛋白含量为8.00％)法建立FGR模型.测定对照组仔鼠和低蛋白组FGR仔鼠生后3、7、14、30、60及90 d(每组每个时间点取雄性仔鼠8只)空腹血浆血糖和空腹血清胰岛素,计算胰岛素抵抗指数及胰岛素敏感指数.采用甲基化特异性聚合酶链反应和逆转录-聚合酶链反应技术测定仔鼠生后7和90 d时肝脏组织PPARγ基因启动子甲基化水平及其mRNA表达情况.采用Pearson相关分析及秩和检验分析肝脏组织中PPARγ基因启动子甲基化及其mRNA表达改变与胰岛素敏感性变化间的关系. 结果 (1)低蛋白组新生仔鼠平均出生体重为(4.92±0.36)g,低于对照组的(6.43±0.59)g(t=14.73,P＜0.05).低蛋白组仔鼠中FGR发生率为88.2％(97/110),其中雄性仔鼠FGR发生率为94.1％(48/51).(2)生后90 d时FGR仔鼠空腹血浆血糖、血清胰岛素和胰岛素抵抗指数显著高于对照组[空腹血浆血糖:(8.95±1.83) mmol/L与(6.21±1.14) mmol/L,t=-3.291,P＜0.05;血清胰岛素:(59.57±9.89) mU/L与(36.10±7.32) mU/L,t=-4.916,P＜0.05;胰岛素抵抗指数:0.967±0.297与0.410±0.135,t=-4.472,P＜0.05)],而胰岛素敏感指数低于对照组仔鼠(-3.043±0.294与-2.172±0.354,t=4.774,P＜0.05).(3)生后7d时,对照组仔鼠与FGR仔鼠PPARγ基因启动子甲基化程度差异无统计学意义(0/8与2/8,Fisher精确概率法,P＞0.05),生后90 d时FGR仔鼠甲基化程度高于对照组仔鼠(8/8与2/8,Fisher精确概率法,P＜0.05).PPARγ基因完全甲基化仔鼠PPARγ基因mRNA相对表达水平最低(27.2±1.6),其次是甲基化与非甲基化共存组(47.3±33.0),完全非甲基化组最高(144.6±21.2),差异均有统计学意义(P均＜0.05).(4)FGR仔鼠生后90 d时PPARγ基因mRNA表达量分别与空腹血浆血糖、血清胰岛素和胰岛素抵抗指数呈负相关(r分别为-0.819、-0.906和-0.860,P均＜0.05),而与胰岛素敏感指数呈正相关(r=0.947,P＜0.05). 结论 PPARγ基因启动子区高甲基化可能抑制其基因转录,从而参与FGR大鼠胰岛素抵抗的发生.     

561例新生儿胰岛素样生长因子-1启动子区域基因多态性观察

目的 检测新生儿胰岛素样生长因子-1(insulin-like growth factor-1,IGF-1)启动子区域737/738位点胞嘧啶腺苷(cytosine-adenosine,CA)重复序列的基因多态性. 方法 选择2010年6月1日至2012年6月30日于北京大学第三医院出生的健康新生儿561例.记录新生儿的性别、出生胎龄、出生体重、身长,并进行胎龄评估.出生后3～5 d清晨空腹采集足跟血,提取DNA,分析IGF-1启动子区域基因多态性.采用x2检验、独立样本t检验、方差分析和Hardy-Weinberg平衡检验进行统计学分析. 结果 561例新生儿中,足月儿413例,早产儿148例；大于胎龄儿92例,适于胎龄儿433例,小于胎龄儿36例.561例共发现7种不同的等位基因及23种不同的基因型.7种等位基因分别为188、190、192、194、196、198和200 bp.最常见的3种基因型为190～192 bp、192～196 bp及192～192 bp,其频率分别为23.2％(130/561)、15.0％(84/561)和12.8％(72/561).CA19纯合基因型(CA19/CA19)、CA19杂合基因型(CA19/CAno19)及CA19突变基因型(CAno19/CAno19)的频率在足月儿和早产儿之间差异均无统计学意义[分别为11.4％(47/413)与16.9％(25/148)、55.9％(231/413)与50.7％(75/148)、32.7％(135/413)与32.4％(48/148),x2=2.96、1.21和0.00,P均＞0.05].CA19/CA19、CA19/CAno19、CAno19/CAno19这3种基因型新生儿的出生胎龄分别为(37.1±2.9)、(37.6±3.1)和(37.4±3.1)周,差异无统计学意义(F=0.54,P=0.58).CA19/CA19在小于胎龄儿中的频率明显高于大于胎龄儿及适于胎龄儿[分别为25.0％(9/36)、7.6％(7/92)及12.9％(56/433),x2=7.01,P=0.03],但CA19/CAno19及CAno19/CAno19基因型频率在大于胎龄儿、适于胎龄儿及小于胎龄儿3组之间差异无统计学意义(CA19/CAno19:x2=1.13,P=0.57；CAno19/CAno19:x2=0.58,P=0.75). 结论 IGF-1启动子区存在基因多态性,CA19等位基因频率与出生胎龄无关.     

胎儿生长受限大鼠胰岛素敏感性的动态变化

目的 探讨胎儿生长受限(fetal growth restriction,FGR)大鼠胰岛素敏感性的变化规律.方法 母鼠受孕后第1天始随机分为对照组和低蛋白组,各10只.低蛋白组孕鼠采用低蛋白饮食法建立FGR模型.低蛋白组仔鼠中出生体重低于对照组仔鼠平均出生体重两个标准差者定为FGR鼠.测定对照组和FGR仔鼠(每组雌雄各8只)生后3、7、14、30、60及90 d空腹血浆血糖(fasting plasma glucose,FPG)及空腹血清胰岛索(fasting serum insulin,FINS),计算胰岛素抵抗指数及胰岛素敏感指数.90 d时测定血甘油三酯、低密度脂蛋白胆固醇、高密度脂蛋白胆固醇和糖化血红蛋白,同时行腹腔葡萄糖耐量实验.结果 (1)低蛋白组仔鼠平均出生体重为(4.92±0.36)g,低于对照组的(6.43±0.59)g,差异有统计学意义(t=14.73,P＜0.05).(2)雄性FGR鼠生后60 d时FPG高于对照组[(9.38±1.57)mmol/L与(5.58士1.24)mmol/L],直至90 d[(8.95±1.83)mmol/L与(6.21±1.14)mmol/L],差异有统计学意义(t=-3.291,P＜0.05);雌性FGR鼠90 d时FPG为(9.08±1.65)mmol/L,高于对照组的(6.73土0.67)mmol/L,差异有统计学意义(t=-3.226,P＜0.05);雄性FGR鼠FINS 30 d时开始高于对照组,直至90 d时;雌性FGR鼠60及90 d时FINS 高于对照组,差异均有统计学意义(P＜0.05);雄性及雌性FGR鼠胰岛素抵抗指数及胰岛素敏感指数分别于30 d及60 d始与对照组相比出现改变,直至90 d,差异有统计学意义(P均＜0.05).腹腔葡萄糖耐量实验结果显示,从0 min始各时间点雄性和雌性FGR鼠血糖均高于对照组,差异均有统计学意义(P＜0.05).(3)生后90 d时,雄性FGR鼠糖化血红蛋白为(7.03±0.54)%,高于对照组的(4.37±0.64)%,差异有统计学意义(t=-8.028,P＜0.05).无论雄性或雌性仔鼠,2组血脂水平差异均无统计学意义(P均＞0.05).结论 FGR鼠在生后早期尚能维持正常的FPG和FINS水平,随着日龄增加,胰岛素敏感性从青年期逐渐降低,直至成年期,而且雄性FGR鼠更易发生胰岛素抵抗.

Abstract：

Objective To investigate the regular pattern of dynamic changes of insulin sensitivity in fetal growth restriction (FGR) rats. Methods Twenty pregnant female rats were randomly divided into two groups as normal-protein group (NP) and low-protein group (LP), which respectively received normal protein diet (20% protein) and low protein diet (8% protein) during pregnancy. Weights of newborns were measured within 6 hours after birth, and the LP offspring whose birth weights were at least 2 standard deviations below the mean of NP offspring (≤2 standard deviations) were defined as FGR rats. At day 3, 7, 14, 30, 60 and 90 after birth, rats were fasted for 12 hours and then angular vein blood was collected to measure fasting plasma glucose (FPG) and fasting serum insulin (FINS) level. At 90 days of age, intraperitoneal glucose tolerance test (IPGTT)was performed; and blood triglyceride ( TG ), low-density lipoprotein cholesterol ( LDL-C ),high-density lipoprotein cholesterol (HDL-C) and glycosylated hemoglobin Alc (HbAlc) were measured. Insulin sensitivity was evaluated by FINS, insulin resistance index (HOMA-IR), insulin sensitivity index (ISI) and IPGTT. Results (1) Birth weights of LP offspring [(4. 92 ± 0. 36) g]were significantly lower than those of NP ones [(6. 43 ± 0. 59) g] (t = 14. 73, P＜0. 05). The incidence of FGR in LP was 88. 2% ; and for the male and female rats, the FGR rate was 94. 1% and 83. 1%, respectively. (2) FPG levels in the male FGR rats were significantly higher than in the NP from the age of 60 days [(9.38 ± 1.57) mmol/L vs (5. 58 ± 1.24) mmol/L] to 90 days [(8. 95 ±1.83) mmol/L vs (6. 21± 1.14) mmol/L] (t=-3. 291, P＜0. 05), while FPG levels in female FGR rats increased significantly only at 90 days of age [(9. 08±1.65) mmol/L vs (6.73±0. 67) mmol/L](t=-3. 226,P＜0. 05). FINS levels were significantly higher in FGR rats than in the NP from the age of 30 days (male FGR rats) or 60 days (female FGR rats) to 90 days (P＜0. 05, respectively).Similarly, HOMA-IR was significantly higher in FGR rats than in the NP at the age of 30 days (male FGR rats) or 60 days (female FGR rats) to 90 days (P＜0. 05, respectively). ISI in male FGR rats showed a reduction in comparison with the NP from the age of 30 to 90 days, while as to the female FGR rats it was significantly lower than in the NP only at 60 days of age and continued to 90 days (P＜0. 05, respectively). IPGTT showed that after injection of glucose, blood glucose at all four points (from 0 min to 120 min) in both male and female FGR rats were higher than that in the NP (P＜0. 05). (3) No significant difference was observed in TG, LDL-C and HDL-C at 90 days of age between the FGR rats and NP ones, while HbA1c in the male FGR rats was significantly higher than that in the NP [(7. 03±0. 54) % vs (4. 37±0. 64)%,t= -8. 028, P＜0. 05]. Conclusions FGR rats are able to maintain glucose balance and normal insulin levels during their earlier age, while insulin sensitivity decreased from adolescence to adulthood. The change of insulin sensitivity is different between male and female FGR rats, and male FGR rats are more likely to develop insulin resistance.     

PTEN基因在宫内发育迟缓大鼠肝脏胰岛素敏感性变化中的作用

目的 通过检测PTEN基因在宫内发育迟缓(IUGR)大鼠肝脏中的表达,探讨PTEN基因在IUGR致胰岛素抵抗(IR)中的意义.方法 通过孕期低蛋白饮食法建立大鼠IUGR模型,检测90d雄性IUGR大鼠胰岛素敏感性,采用反转录(RT)-PCR技术检测90 d IUGR组及对照组仔鼠肝脏PTEN基因mRNA表达水平,Western blot检测肝脏组织中丝氨酸/苏氨酸激酶(AKT)蛋白及磷酸化AKT蛋白表达水平.采用SPSS 13.0软件进行统计学处理.结果 与对照组比较,IUGR雄性仔鼠平均出生体质量显著降低(t=14.73,P＜0.05),空腹血糖显著升高(t=-3.11,P=0.011),空腹胰岛素显著升高(t=-5.01,P=0.001),胰岛素抵抗指数显著升高(t=-3.06,P=0.013),胰岛素敏感指数显著降低(t=2.80,P=0.019),PTEN基因mRNA表达显著升高(t=-2.40,P =0.04),AKT蛋白表达虽然无统计学差异,但磷酸化AKT蛋白表达显著下降(t=3.02,P=0.01),PTEN与胰岛素抵抗指数呈正相关(r=0.928,P ＜0.05),与磷酸化AKT的表达呈负相关(r=-0.411,P＜0.05).结论 PTEN可能是IUGR致IR的重要调节分子之一.     

阿昔洛韦治疗传染性单核细胞增多症的Meta分析

目的:系统评价阿昔洛韦治疗传染性单核细胞增多症(IM)的有效性及安全性,为临床应用阿昔洛韦治疗IM提供参考依据。方法:以阿昔洛韦、IM为关键词,检索PubMed、EMbase、The Cochrane Library、VIP、CNKI和Wanfang Data,收集阿昔洛韦治疗IM的随机对照试验(RCT),检索时限均为建库至2015年8月。由两位研究者按照纳入与排除标准独立进行文献筛选、资料提取和评价纳入研究的偏倚风险后,应用RevMan5.3软件进行Meta分析。结果:共纳入6个RCT,384例患儿。Meta分析结果显示:与常规及利巴韦林治疗IM比较,阿昔洛韦可缩短患儿退热时间[MD=-2.71,95% CI(-3.05,-2.36)]、咽峡炎改善时间[MD=-2.66,95% CI(-3.55,-1.77)]、肿大淋巴结缩小时间[MD=-3.43,95% CI(-3.90,-2.96)]及异型淋巴细胞计数减少时间[MD=-3.16,95% CI(-4.25,-2.08)],差异有统计学意义。结论:阿昔洛韦可缩短IM患儿发热时间,促进咽峡炎症状改善、促进肿大淋巴结回缩及减少异型淋巴细胞计数。由于纳入文献研究质量不高,上述结论有待更多高质量研究进一步证实。     

低出生体重儿婴儿期生长速度与胰岛素敏感性的关系

【目的】 探讨低出生体重儿婴儿期生长速度与胰岛素敏感性的关系。 【方法】 将全部入选对象分为低出生体重儿组(low birth weight,LBW)和正常对照组(normal control,NC),并随访1年。766例新生儿纳入研究,共计628例完成1年随访。分别在生后42 d、4、6、8、10个月和12个月共计随访6次,进行体格测量,并在6个月和12个月随访当日测定血清胰岛素(fasting insulin,FI)和血糖水平。计算出生体格Ponderal指数,随访中计算体质指数(body mass index,BMI)以及内稳态模式评估值(homeostasis model assessment,HOMA)评价胰岛素敏感性。 【结果】 LBW组与NC组相比,LBW组婴儿在12个月内的每一个监测点生长发育水平始终低于NC组,但是由体重和身长的Z-score变化可以看到,虽然两组间在12个月时差异仍然显著,但是Z-score值在不断减小;最后,由1年内Z-score的变化即ΔZ-score可见,在婴儿期,LBW组婴儿体重及身长均快速增长,其增长速度显著高于NC组婴儿,但是,在12个月时仍未能追上NC组婴儿。6月龄时,两组间胰岛素敏感性无差异,12个月龄时,LBW组FI和HOMA值较高,提示此阶段胰岛素敏感性相对差。 【结论】 低出生体重儿在12个月内生长发育速度快于正常体重儿,在12个月时体重、身长和BMI值仍低于正常体重儿;低出生体重儿在婴儿期末已经表现出胰岛素敏感性相对差。