孕妇外周血中胎儿DNA水平检测在子痫前期诊断中的应用

目的探讨孕妇外周血中胎儿DNA水平检测在子痫前期诊断中的应用价值。方法选择30例子痫前期孕妇为子痫前期组(其中轻度18例,重度12例),另选择30例正常孕妇作为对照组,两组孕妇分别于孕20周、孕晚期(子痫前期组孕33周+3、对照组孕34周+3)、分娩后1、3、6 h取外周血,采用荧光定量PCR检测外周血中Y染色体上的性别决定基因(SRY基因)胎儿DNA水平(B超确定两组孕妇所妊娠的胎儿均为男性);放射免疫法检测两组孕妇孕晚期内皮素水平。结果(1)子痫前期组孕20周时的胎儿DNA水平为(316±61)copy/m l,其中轻度、重度患者分别为(266±79)、(396±91)copy/m l;对照组孕妇为(165±43)copy/m l,子痫前期组及轻度、重度患者明显高于对照组,两组比较,差异有统计学意义(P<0.01)。(2)子痫前期组孕晚期胎儿DNA水平为(970±413)copy/m l,其中轻度、重度患者分别为(758±357)、(1285±573)copy/m l,对照组孕妇为(319±99)copy/m l,子痫前期组及轻度、重度患者明显高于对照组,两组比较,差异有统计学意义(P<0.01)。(3)子痫前期组产后1、3、6 h胎儿DNA水平分别为(139±45)、(76±31)、(44±13)copy/m l,其中轻度患者分别为(102±42)、(57±25)、(36±12)copy/m l,重度患者分别为(209±51)、(97±40)、(52±17)copy/m l;对照组分别为(33±13)、(9±5)、0 copy/m l。子痫前期组及轻度、重度患者明显高于对照组,两组比较,差异有统计学意义(P<0.01)。(4)子痫前期组内皮素水平为(80±18)ng/L,其中轻度患者为(74±14)ng/L,重度患者为(89±32)ng/L;对照组为(50±11)ng/L,子痫前期组及轻度、重度患者明显高于对照组,两组比较,差异有统计学意义(P<0.01)。(5)子痫前期组胎儿DNA水平与内皮素水平呈正相关关系(r=0.748,P<0.01)。结论孕妇外周血胎儿DNA水平变化可以作为预测和诊断子痫前期发病与疾病程度的一个指标。     

子痫前期血清脂联素水平变化与胰岛素抵抗的关系

目的 探讨子痫前期患者血清脂联素水平变化及其与胰岛素抵抗的关系.方法 选取2006年1月至2008年10月于解放军第202医院妇产科住院分娩的子痫前期患者110例为研究时象,其中轻度子痫前期患者58例,重度子痫前期患者52例,另取68例正常孕妇作为对照组.采用酶联免疫吸附法(ELIsA)测定各组孕妇血清脂联素水平,同时测定各组孕妇空腹血糖、空腹胰岛素水平,并计算胰岛素抵抗指数,以评价胰岛素抵抗程度.结果 轻度子痫前期患者脂联素水平(15.59±2.42)mg/L明显高于对照组(11.52±1.27)mg/L(P<0.05),重度子痫前期患者脂联素水平(20.47±3.09mg/L)明显高于对照组及轻度子痫前期组(P<0.01).空腹血糖、空腹胰岛素水平及胰岛素抵抗指数在各组之间无统计学意义(P>0.05).在子痫前期患者中血清脂联素水平与空腹胰岛素水平及胰岛素抵抗指数显著负相关(r值分别为-0.628,-0.389,P值分别为0.002,0.009).结论 脂联素可能参与了子痫前期的发生、发展过程,脂联素可能成为反映胰岛素抵抗严重程度的指标.     

血清可溶性血管内皮生长因子受体与子痫前期发病的关系

目的探讨血清中可溶性血管内皮生长因子受体1(sFlt-1)的变化及其与子痫前期发病的关系。方法(1)应用半定量RT-PCR技术检测10例重度子痫前期患者(子痫前期组)及10例足月正常妊娠妇女(正常妊娠组)的胎盘组织中sFlt-1mRNA表达水平。(2)应用酶联免疫吸附试验(ELISA)法测定35例重度子痫前期患者(子痫前期1组)及35例正常足月妊娠妇女(正常妊娠1组)外周血中sFlt-1水平。(3)ELISA测定20例重度子痫前期患者(子痫前期2组)及20例正常足月妊娠妇女(正常妊娠2组)胎盘附着处子宫静脉血中sFlt-1水平。(4)ELISA测定10例早孕(早孕组)及10例中孕(中孕组)妇女外周血中sFlt-1水平。结果(1)子痫前期组胎盘组织中sFlt-1mRNA表达水平为0.95±0.04,明显高于正常妊娠组的0.64±0.15,两组比较,差异有统计学意义(P<0.01)。(2)子痫前期1组孕妇外周血清中sFlt-1水平为(5640±3191)ng/L,明显高于正常妊娠1组的(2194±635)ng/L,两组比较,差异有统计学意义(P<0.01)。(3)子痫前期2组孕妇子宫静脉血清中sFlt-1水平为(7673±2296)ng/L,明显高于正常妊娠2组的(3057±785)ng/L,两组比较,差异有统计学意义(P<0.01)。(4)早、中孕组孕妇外周血清中sFlt-1水平分别为(32±20)ng/L及(994±302)ng/L。结论(1)子痫前期患者外周血中sFlt-1水平明显增高;(2)血清中sFlt-1水平随孕周增加而升高,并可能与子痫前期的发病有关。     

子痫前期患者血清及胎盘组织中人类白细胞抗原G的表达研究

目的:检测正常晚期妊娠妇女及子痫前期患者胎盘组织HLA-G的表达及血清中sHLA-G的浓度,探讨HLA-G在子痫前期发病中的临床意义。方法:用半定量逆转录-聚合酶链技术(RT-PCR)检测37例正常晚期妊娠妇女(正常妊娠组)及41例子痫前期患者(轻度20例,重度21例)胎盘组织中HLA-G mRNA的表达;并用ELISA检测血清sHLA-G浓度。结果:(1)子痫前期胎盘组织中HLA-G mRNA表达水平分别为:轻度0.402±0.104、重度0.329±0.09,明显低于正常妊娠组的0.628±0.117(P<0.01),轻、重度差异亦有统计学意义(P<0.05)。(2)子痫前期血清sHLA-G浓度:轻度45.5±11.9u/ml,重度31.2±10.3u/ml,均明显低于正常妊娠组的105.7±12.5u/ml(P<0.01),轻重度差异亦有统计学意义(P<0.01)。(3)子痫前期患者血清sHLA-G浓度与胎盘组织HLA-G mRNA表达水平呈正相关(r=0.702,P<0.01)。结论:子痫前期血清sHLA-G浓度及胎盘组织中HLA-G表达水平均明显降低,可能与子痫前期发病及病情轻重程度相关。     

胰岛素样生长因子1及胰岛素样生长因子结合蛋白1表达与妊娠期高血压疾病发病的关系

目的探讨胰岛素样生长因子1(IGF-1)与胰岛素样生长因子结合蛋白1(IGFBP-1)在妊娠期高血压疾病发病中的作用。方法采用酶联免疫吸附法(ELISA)及免疫组化方法检测60例妊娠期高血压疾病患者(妊娠期高血压疾病组,其中妊娠期高血压20例、轻度子痫前期19例、重度子痫前期21例)及18例正常妊娠妇女(对照组)的血清及胎盘组织中IGF-1及IGFBP-1的水平,并分析妊娠期高血压疾病组患者血清中IGF-1水平与胎盘组织中IGFBP-1的相关性。结果(1)血清IGF-1水平:妊娠期高血压疾病组为(229±100)μg/L,明显低于对照组的(336±120)μg/L,两组比较,差异有统计学意义(P<0.01)。妊娠期高血压患者血清中IGF-1水平为(303±80)μg/L,轻度子痫前期患者为(233±77)μg/L,重度子痫前期患者为(155±73)μg/L。3者间比较,差异有统计学意义(P<0.05)。(2)胎盘组织中IGF-1阳性率:妊娠期高血压疾病组为48%(29/60),明显低于对照组的83%(15/18),两组比较,差异有统计学意义(P<0.01);轻、重度子痫前期患者明显低于对照组(P<0.05,P<0.01)。(3)血清中IGFBP-1水平:妊娠期高血压疾病组为(161±90)μg/L,明显高于对照组的(98±75)μg/L,两组比较,差异有统计学意义(P<0.01)。妊娠期高血压患者为(97±73)μg/L,轻度子痫前期患者为(157±69)μg/L,重度子痫前期患者为(225±81)μg/L。3者间比较,差异有统计学意义(P<0.05)。(4)胎盘组织中IGFBP-1阳性率:妊娠期高血压疾病组为77%(46/60),明显高于对照组的39%(5/18),两组比较,差异有统计学意义(P<0.01);轻、重度子痫前期患者明显高于对照组(P<0.05,P<0.01)。(5)相关性:妊娠期高血压疾病组患者血清及胎盘组织中IGF-1水平分别与相应部位的IGFBP-1水平均呈负相关(r=-0.269,P<0.05;r=-0.396,P<0.01)。血清中IGFBP-1水平与胎盘组织中IGFBP-1表达水平呈正相关(r=0.388,P<0.01)。结论孕妇血清及胎盘组织中IGF-1、IGFBP-1水平变化与妊娠期高血压疾病发病及病情发展有关。     

血清中脂联素水平变化及脂肪组织中脂联素mRNA表达与子痫前期发病的关系

-0.446(P均<0.05);对照组孕妇大网膜脂肪组织中脂联素mRNA表达水平与孕前体重指数呈明显负相关(r=-0.436,P<0.05).结论 子痈前期孕妇血清脂联素水平降低,提示其可能参与了子痫前期的病理生理过程;而子痫前期孕妇大网膜脂肪组织中脂联素mRNA表达水平显著下降,可能是子痫前期孕妇血清脂联素水平下降的主要原因.     

肥胖儿童脂联素和血脂检测及其相关性

目的探讨血清脂联素(adiponectin)、血脂在肥胖儿及正常儿体内的变化情况及脂联素与体重指数(BMI)、体脂肪率(FATR)、血脂等相关关系。 方法测定肥胖儿及正常儿各30例的血清脂联素、甘油三酯(TG)、胆固醇(TC)、高密度脂蛋白胆固醇(HDL C)、低密度脂蛋白胆固醇(LDL C)等，并进行两组之间的比较。 结果肥胖儿组脂联素(10.06±4.87)mg/L明显低于正常对照组(13.18±5.18)mg/L，两者差异有显著性意义(P<0.05)，肥胖儿组低密度脂蛋白胆固醇(3.10±1.08)mmol/L明显高于正常对照组(2.48±0.71)mmol/L，两者差异有显著性意义(P<0.05)。肥胖儿组甘油三酯(2.54±1.11)mmol/L明显高于正常对照组(1.75±0.79)mmol/L，两者差异有非常显著意义(P<0.01)，肥胖儿组脂联素和体重指数BMI呈负相关(r=-0.53,P=0.00)。 结论肥胖组较非肥胖对照组血中脂联素水平降低，血脂水平异常。     

妊高征患者血清瘦素水平变化的研究

目的 :探讨妊娠高血压综合征 (妊高征 )患者血清瘦素 (leptin)水平的变化及其与妊高征发病的关系。方法 :采用放射免疫分析法测定了 36例妊高征患者 (妊高征组 )和 30例正常孕妇 (正常妊娠组 )产前及产后血清瘦素水平。结果 :中、重度妊高征患者产前瘦素水平为 15 .19± 6 .74 ng/ ml明显高于正常妊娠组的 10 .11± 2 .80 ng/ m l(P<0 .0 5 ) ;轻度妊高征组患者产前瘦素水平 12 .77± 4 .6 8ng/ ml与正常妊娠组比较 ,差异无显著性 (P>0 .0 5 )。妊高征患者产后瘦素水平为 5 .91± 2 .6 8ng/ ml,与产前 14 .5 6± 6 .30 ng/ ml相比 ,差异显著 (P<0 .0 5 )。妊高征组产后瘦素水平与正常妊娠组 5 .74± 2 .38ng/ ml相比 ,差异无显著性。结论 :妊高征患者血清瘦素水平升高 ,与妊高征的发生有关     

可溶性血管内皮生长因子受体1在子痫前期患者胎盘组织中的表达及意义

目的探讨可溶性血管内皮生长因子受体1(sFlt-1)在子痫前期患者胎盘组织中的mRNA及蛋白表达水平变化及其意义。方法(1)采用免疫组化方法及RT-PCR技术分别检测30例子痫前期患者(子痫前期组,其中轻度子痫前期11例,重度子痫前期19例)及45例健康孕妇(对照组,其中早期妊娠18例、中期妊娠12例、晚期妊娠15例)胎盘组织中sFlt-1的蛋白及mRNA表达水平。(2)采用酶联免疫吸附试验(ELISA)测定各组孕妇血清中血管内皮生长因子(VEGF)及sFlt-1水平。结果(1)子痫前期组胎盘组织中sFlt-1 mRNA表达水平为0．90±0．11,对照组晚期妊娠妇女为0．80±0．06,两者比较,差异有统计学意义(P<0．01)。子痫前期组重度患者为0．93±0．12,子痫前期组轻度患者为0．85±0．05,两者比较,差异也有统计学意义(P<0．05)。(2)sFlt-1蛋白在子痫前期组患者胎盘组织中的表达水平为0．156±0．008,对照组中晚期妊娠妇女为0．143±0．009,两者比较,差异有统计学意义(P<0．01);子痫前期组重度患者sFlt-1蛋白表达水平为0．159±0．008,子痫前期组轻度患者为0．151±0．005,两者比较,差异也有统计学意义(P<0．05)。(3)子痫前期组孕妇血清VEGF、sFlt-1水平分别为(19．3±2．9)ng／L、(30．2±13．7)μg／L,对照组晚期妊娠妇女为(30．2±3．1)ng／L、(7．4±3．1)μg／L,两者比较,差异有统计学意义(P<0．01)。(4)对照组孕妇血清sFlt-1水平与胎盘sFlt-1蛋白及mRNA表达水平呈正相关关系(r=0．439,P<0．01;r=0．314,P< 0．05);子痫前期组孕妇血清sFlt-1水平与胎盘sFlt-1蛋白及mRNA表达水平也呈正相关关系(r= 0．383,r=0．372;P均<0．05)。结论子痫前期患者胎盘组织中sFlt-1 mRNA表达水平上调及sFlt-1蛋白过度表达,可引起循环中sFlt-1水平升高,从而参与子痫前期的病理生理过程。     

妊娠期高血压疾病孕妇瘦素与红细胞膜Ca~(2+)-ATP酶活性的研究

目的:探讨瘦素、红细胞膜Ca2+-ATP酶活性在妊娠期高血压疾病发病中的意义及相互关系。方法:采用放射免疫法测定38例妊娠期高血压疾病患者,36例正常孕妇的血清瘦素。采用生化方法提取红细胞膜,测定红细胞膜Ca2+-ATP酶活性。结果:妊娠期高血压疾病患者血清瘦素水平明显高于对照组(15.95±5.10ng/m l vs 11.33±2.93ng/m l),红细胞膜Ca2+-ATP酶活性明显低于对照组[1.38±0.19μmol.pi/(mg.h)vs 1.83±0.38μmol.pi/(mg.h)](P<0.01)。妊娠期高血压疾病患者血清瘦素与红细胞膜Ca2+-ATP酶活性呈负相关(r=-0.63)。结论:血清瘦素水平与妊娠期高血压疾病的发生有关;妊娠期高血压疾病患者红细胞膜Ca2+-ATP酶活性降低引起细胞内游离Ca2+浓度升高,导致妊娠期高血压疾病发生;妊娠期高血压疾病患者血清瘦素水平与红细胞膜Ca2+-ATP酶活性呈负相关,两者共同参与妊娠期高血压疾病的发病。     

Serum levels of leptin, insulin-like growth factor-I and insulin-like growth factor binding protein-3 in women with pre-eclampsia, and their relationship to insulin resistance.

The present study was carried out to compare serum levels of leptin, insulin-like growth factor-I (IGF-I), insulin-like growth factor binding protein-3 (IGFBP-3), homeostasis model assessment--(pancreatic beta-cell function) (HOMA-(%B)) and homeostasis model assessment--(tissue insulin sensitivity) (HOMA-(%S)) in women with mild and severe pre-eclampsia and normotensive pregnant women; and to evaluate the possible relationships between these parameters in the pathogenesis of pre-eclampsia. Seventy-three women were divided into three groups: group A consisted of 20 normotensive pregnant women (NPW); group B consisted of 25 women with mild pre-eclampsia (MPE); and group C consisted of 28 women with severe pre-eclampsia (SPE). Serum level of leptin was measured by enzyme immunoassay using a commercial kit. Serum levels of IGF-I and IGFBP-3 were measured with a two-site immunoradiometric assay. Serum level of insulin was measured by the electrochemiluminescence immunoassay method. HOMA used indices of pancreatic beta-cell function and tissue insulin sensitivity. Differences between groups were compared by one-way analyses of variance and the post hoc Tukey-HSD test for multiple comparisons; however, when a variable was not normally distributed, the Mann-Whitney U test was used. Associations between variables were tested using Pearson's coefficient of correlation. Birth weight was significantly lower (p < 0.001) in the MPE and SPE groups than in the NPW group. Serum levels of leptin and insulin in women with SPE and MPE were significantly higher (p < 0.001) than in NPW. Serum levels of IGF-I and IGFBP-3 were significantly lower in women with SPE and MPE compared with NPW (p < 0.001). The mean HOMA-(%B) level in women with SPE and MPE was significantly higher than in NPW (p < 0.001), whereas the mean HOMA-(%S) level in women with SPE and MPE was significantly lower than in NPW (p < 0.001). In the SPE group, systolic blood pressure correlated significantly with serum levels of IGF-I and leptin (r = 0.375, p < 0.05 and r = 0.495, p < 0.01, respectively). A negative correlation between mean HOMA-(%S) level and serum IGFBP-3 level was noted (r = -0.357, p < 0.05). There was a positive correlation between serum level of IGF-I and mean HOMA-(%B) level in mildly pre-eclamptic women (r = 0.541, p < 0.01). We conclude that pre-eclampsia is associated with insulin resistance; and that existing hyperinsulinemia and insulin resistance in women with pre-eclampsia seem not to correlate with leptin and birth weight, but may correlate positively with IGF-1 and IGFBP-3. Therefore we think that hyperleptinemia, low IGF-I or IGFBP-3, and insulin resistance may contribute to the pathogenesis of pre-eclampsia.     

Serum levels of leptin,insulin-like growth factor-I and insulin-like growth factor binding protein-3 in women with pre-eclampsia,and their relationship to insulin resistance

The present study was carried out to compare serum levels of leptin, insulin-like growth factor-I (IGF-I), insulin-like growth factor binding protein-3 (IGFBP-3), homeostasis model assessment–(pancreatic β-cell function) (HOMA-(%B)) and homeostasis model assessment–(tissue insulin sensitivity) (HOMA-(%S)) in women with mild and severe pre-eclampsia and normotensive pregnant women; and to evaluate the possible relationships between these parameters in the pathogenesis of pre-eclampsia. Seventy-three women were divided into three groups: group A consisted of 20 normotensive pregnant women (NPW); group B consisted of 25 women with mild pre-eclampsia (MPE); and group C consisted of 28 women with severe pre-eclampsia (SPE). Serum level of leptin was measured by enzyme immunoassay using a commercial kit. Serum levels of IGF-I and IGFBP-3 were measured with a two-site immunoradiometric assay. Serum level of insulin was measured by the electrochemiluminescence immunoassay method. HOMA used indices of pancreatic β-cell function and tissue insulin sensitivity. Differences between groups were compared by one-way analyses of variance and the post hoc Tukey–HSD test for multiple comparisons; however, when a variable was not normally distributed, the Mann–Whitney U test was used. Associations between variables were tested using Pearson's coefficient of correlation. Birth weight was significantly lower (p?<?0.001) in the MPE and SPE groups than in the NPW group. Serum levels of leptin and insulin in women with SPE and MPE were significantly higher (p?<?0.001) than in NPW. Serum levels of IGF-I and IGFBP-3 were significantly lower in women with SPE and MPE compared with NPW (p?<?0.001). The mean HOMA-(%B) level in women with SPE and MPE was significantly higher than in NPW (p?<?0.001), whereas the mean HOMA-(%S) level in women with SPE and MPE was significantly lower than in NPW (p?<?0.001). In the SPE group, systolic blood pressure correlated significantly with serum levels of IGF-I and leptin (r?=?0.375, p?<?0.05 and r?= 0.495, p?<?0.01, respectively). A negative correlation between mean HOMA-(%S) level and serum IGFBP-3 level was noted (r?=?–0.357, p?<?0.05). There was a positive correlation between serum level of IGF-I and mean HOMA-(%B) level in mildly pre-eclamptic women (r?=?0.541, p?<?0.01). We conclude that pre-eclampsia is associated with insulin resistance; and that existing hyperinsulinemia and insulin resistance in women with pre-eclampsia seem not to correlate with leptin and birth weight, but may correlate positively with IGF-1 and IGFBP-3. Therefore we think that hyperleptinemia, low IGF-I or IGFBP-3, and insulin resistance may contribute to the pathogenesis of pre-eclampsia.     

Are serum chemerin levels different between obese and non-obese polycystic ovary syndrome women?

The objective of this study is to measure serum chemerin levels in women with polycystic ovary syndrome (PCOS) and assess their relationship with clinical, metabolic, and hormonal parameters. One hundred eighteen PCOS women and 114 healthy women were recruited in this study. Their blood pressure, body mass index (BMI), waist circumference and waist-to-hip ratio (WHR), fasting insulin (FIN), fasting plasma glucose (FPG), blood serum sex hormone, and blood lipid were measured. Serum chemerin, leptin, and adiponectin were measured by ELISA. Serum chemerin was significantly higher in the obese PCOS group (47.62?±?11.27?ng/mL) compared with non-obese PCOS (37.10?±?9.55?ng/mL) and the obese (33.71?±?6.17?ng/mL) and non-obese (25.78?±?6.93?ng/mL) control groups (p?p?相似文献   

Adiponectin, leptin and lipid profiles evaluation in oral contraceptive pill consumers

Background

The aim of this study was to evaluate serum lipid profiles, leptin and adiponectin levels in women with a normal menstrual cycle receiving low-dose (LD) combined oral contraceptive pill (COC) (levonorgestrel 0.15?mg, ethinyl-estradiol 0.03?mg).

Study design

Serum adiponectin and leptin concentrations were measured by enzyme-linked immunosorbent assay (ELISA), and spectrophotometric assay was used for serum lipid and lipoprotein profiles assay in 50 healthy women with normal menstrual cycles who served as the control group and 50 women taking COCs. Unpaired t test and Chi-square test were used for comparison of variables between oral contraceptive users and non-oral contraceptive users.

Results

Serum adiponectin and leptin levels were changed in COC consumers. The data obtained for adiponectin in COC consumers (6.6?±?4.06?μg/ml) were significantly lower (?27.4%, P?=?0.004) than control group (9.1?±?5.09?μg/ml). The difference between the serum leptin concentration of the control group (11.5?±?6.9?ng/ml) and women receiving COCs (14.1?±?6.7?ng/ml) was not significant (+18.4%, P?=?0.083). There was nonsignificant difference between HDL levels of subjects taking COC (44.02?±?10.7?mg/dl) and control group (49.4?±?14.3?mg/dl). The LDL levels of COC consumer (131.40?±?66.40?mg/dl) was significantly higher (P?=?0.002) than controls (102.30?±?44.0?mg/dl). The serum cholesterol concentration of women receiving COC (193.2?±?70.4?mg/dl) was significantly higher (P?=?0.05) than controls (172.8?±?49.6?mg/dl). The age of COC consumption and the duration of intake of COCs beyond 36?months had no significant effect on the adiponectin and leptin concentrations.

Conclusion

LD COC uptake results in a significant decrease in serum adiponectin concentration, nonsignificant increase in leptin levels and a more atherogenic lipid profile by significantly increasing LDL and nonsignificantly decreasing HDL concentrations. These findings suggested that COC may reduce or stimulate the adiponectin and leptin concentrations, respectively. This might be due to an effect of these pills on adipocyte maturation via inhibition or stimulation of the synthesis of new adiponectin and leptin molecules or may be a result of the increased frequency of a particular allele of the adiponectin and leptin. It is suggested that these alterations in adiponectin and leptin concentrations and lipid profiles may be related to their probable effects in response to various pathological and physiological properties of COC or its metabolites. It seems that probably free radicals produced during metabolism of COCs change the amounts of adipokines and atherogenic lipids.     

The relationship between plasma levels of leptin and androgen in healthy and preeclamptic pregnant women

BACKGROUND: To clarify the role of leptin and androgens in the pathogenesis of preeclampsia, we wanted to assess role of maternal leptin in women with severe and mild preeclampsia and the effects of sex steroid hormones on leptin production. METHODS: The groups consisted of 40 healthy pregnant women (HPW) as well as 55 pregnant women with severe preeclampsia (SPE) and 41 pregnant women with mild preeclampsia (MPE). No significant differences were observed between the three groups regarding age, gestational age and body mass index (BMI). Plasma leptin, total testosterone (T), estradiol (E(2)), dehydroepiandrosterone sulfate (DHEAS) and androstenedione (A) levels were measured. Statistical analysis was achieved with one-way analysis of variance (anova) followed by post hoc multiple comparisons with the Tukey honestly significant difference (HSD) test by using SPSS for Windows statistical computer program, and the Pearson's coefficient of correlation was calculated. RESULTS: The plasma level of leptin was significantly increased in the SPE and MPE groups (p < 0.001), whereas the plasma level of T was significantly increased only in the SPE group (p < 0.001). However, there was no significant difference in plasma levels of DHEAS among the three groups (p < 0.05). The plasma level of A was significantly decreased in the MPE group (p < 0.05). There was no significant difference in the plasma level of E(2) in the MPE and SPE groups (p < 0.05). There was a significant positive correlation between the plasma levels of leptin and E(2) in the MPE group (r = 0.41, p < 0.001). CONCLUSION: We concluded that the elevated plasma levels of leptin and testosterone could contribute to the endothelial dysfunction involved in the pathogenesis of preeclampsia, and that estradiol might lead to an increase in the plasma levels of leptin.     

脂联素和胰岛素与胎儿生长的关系

目的:探讨脂联素,胰岛素与胎儿生长发育的关系。方法:选取21例分娩生长受限胎儿(FGR组)、21例分娩巨大儿(巨大儿组)及21例分娩正常儿(对照组)的产妇,抽取3组产妇分娩后肘静脉血及其新生儿脐静脉血.分离血清。采用双抗体夹心酶联免疫吸附法和放射免疫法测定3组产妇血清及新生儿脐静脉血清中脂联素和胰岛素的水平。结果:FGR组产妇血清脂联素水平明显低于对照组及巨大儿组(P<0.01);FGR组新生儿脐血清脂联素水平明显低于对照组及巨大儿组(P<0.05);3组产妇血清中脂联素水平均明显低于新生儿脐血清中脂联素水平(P<0.01)。FGR组胎盘重量明显低于对照组及巨大儿组(P<0.01);3组产妇血清及新生儿脐血血清中胰岛素水平差异无显著性(P>0.05)。3组产妇血清脂联素水平与胰岛素水平无相关(P>0.05);3组新生儿脐血清脂联素水平与胰岛素水平呈明显负相关性(P<0.05);3组产妇血清脂联素水平与新生儿脂联素水平无相关(P>0.05);3组产妇血清胰岛素水平和新生儿脐血胰岛素水平无相关性(P>0.05)。3组新生儿脐血清脂联素水平与新生儿出生体重、胎盘重量、新生儿头围、身长、体重/身长比呈明显正相关关系(P<0.05);3组新生儿脐血清胰岛素水平、产妇血清脂联素水平、产妇血清胰岛素水平与新生儿出生体重、胎盘重量、头围、身长、体重/身长比均无相关性。结论:脐血中的脂联素、胰岛素在胎儿宫内生长和发育过程中可能起重要的调节作用,可作为评价胎儿生长发育及体内脂肪储备状态的临床指标之一。胎儿自身分泌的脂联素与胎儿生长关系密切。     

二甲双胍对高胰岛素血症肥胖儿童糖代谢和血清脂源性激素的影响

目的观察二甲双胍治疗对高胰岛素血症肥胖患儿血清脂源性激素脂联素、抵抗素、瘦素水平的影响。 方法2004 01—2005 02将武汉市儿童医院和同济医院54例高胰岛素血症肥胖患儿分为轻、中度肥胖组及重度肥胖组,均以二甲双胍治疗12周，测量治疗前后体重、空腹血糖、空腹胰岛素及脂源性激素脂联素、瘦素、抵抗素的变化。 结果治疗前轻、中度肥胖组和重度肥胖组高胰岛素血症患儿空腹血糖水平与健康对照组比较差异无显著性(P>0.05)，血清胰岛素、瘦素、抵抗素及胰岛素抵抗指数(HOMA IR)均高于健康对照组(P<0.01)，脂联素水平明显低于健康对照组(P<0.01)。二甲双胍治疗12周后与治疗前相比,血清胰岛素水平、胰岛素抵抗指数明显降低(P<0.01)，轻、中度肥胖组及重度肥胖组血清瘦素水平分别由治疗前的(24.3±1.8)μg/L、(30.2±5.1)μg/L降低为治疗后的(19.6±6.3)μg/L、(24.7±5.3)μg/L，差异有统计学意义；抵抗素水平分别由治疗前的(16.5±6.0)μg/L、(22.3±5.2)μg/L升高为(22.0±5.1)μg/L、(30.6±11.7)μg/L，差异有统计学意义；轻、中度肥胖组和重度肥胖组血清脂联素水平治疗前分别为(8.4±3.2)mg/L、(6.5±1.2)mg/L，治疗后分别为(8.9±2.3)mg/L、(7.03±3.0)mg/L，治疗前后相比,P>0.05。体重指数(BMI)下降,但差异无显著性。 结论二甲双胍能显著改善肥胖患儿胰岛素抵抗。降低血清瘦素水平可能是其改善胰岛素抵抗机制之一，但在对脂源性激素脂联素、抵抗素水平的改善上，有其局限性。     

Maternal serum adiponectin concentration in gestational diabetes

Aim. Adiponectin is an insulin sensitizing protein. Because gestational diabetes mellitus is associated with insulin resistance, we compared serum adiponectin levels in women with gestational diabetes mellitus and healthy pregnant women.

Study design. Twenty-nine women with gestational diabetes and 26 women with impaired glucose tolerance were compared with 27 normal pregnant women in control group. Controls were matched for gestational age, age and body mass index (BMI) before pregnancy with two other groups. At 28 weeks of gestation serum concentration of adiponectin, insulin and insulin resistance (calculated by the homeostasis model assessment) were measured in three groups.

Main findings. The serum adiponectin level in gestational diabetes (6379.31 ± 1934.90 ng/ml), was significantly lower than the impaired glucose tolerance test (7384.61 ± 1626.70 ng/ml) and control groups (7962.96 ± 2667.20 ng/ml),(p = 0.02). Serum level of insulin and HOMA index in gestational diabetes were higher than the normal group (p > 0.05). In patients with gestational diabetes, there was a significant correlation between serum adiponectin level and BMI before pregnancy (r = ?0.531, p = 0.013). Also, the correlation between maternal serum adiponectin levels and neonatal birth weight was not significant (r = ?0.07, p value = 0.73).

Conclusion. Our data show that serum adiponectin level was significantly lower in gestational diabetes in comparison with healthy pregnant women.     

MIF和子痫前期炎症反应机制的关系

目的研究子痫前期胎盘组织炎症反应情况及巨噬细胞移动抑制因子（MIF）的表达,探讨MIF在子痫前期炎症反应中的作用。方法选取住院分娩的子痫前期孕产妇53例,其中轻度子痫前期孕产妇25例（轻度子痫前期组）,重度子痫前期孕产妇28例（重度子痫前期组）。另选取同期正常妊娠晚期孕产妇30例为对照组。采用逆转录（RT）PCR技术检测三组孕产妇胎盘组织中MIFmRNA的表达;采用免疫比浊法检测三组孕产妇血浆中CRP水平;采用ELISA方法检测三组孕产妇血浆中（TNF-α）、IL-6浓度。并对轻度及重度子痫前期组孕产妇血浆中CRP水平与胎盘组织中MIFmRNA表达的相关性进行分析。结果①三组孕产妇胎盘组织中均有MIF的表达,轻度子痫前期组孕产妇胎盘组织中MIFmRNA的水平为（0.84±0.13）,重度子痫前期组为（1.05±0.11）,两组比较,差异有统计学意义（P〈0.01）。对照组孕产妇胎盘组织中MIFmRNA为（0.70±0.12）,明显低于轻度及重度子痫前期组,差异均有统计学意义（P〈0.01）;②轻度子痫前期组孕产妇血浆CRP、（TNF-α）、IL-6浓度分别为（14.99±6.85）mg/L、（14.76±3.67）pg/ml、（24.68±10.13）pg/L,重度子痫前期组孕产妇血浆CRP、（TNF）、IL-6浓度分别为（21.16±8.89）mg/L、（19.66±6.13）pg/ml、（30.91±14.34）pg/L,差异有统计学意义（P〈0.01）;对照组孕产妇血浆CRP、（TNF）、IL-6浓度分别为（4.71±1.76）mg/L、（9.94±2.53）pg/ml、（14.14±5.06）pg/L,明显低于轻度及重度子痫前期组,差异有统计学意义（P〈0.01）;③轻度及重度子痫前期组孕产妇血浆中CRP水平与胎盘组织中MIFmRNA表达水平呈正相关（r=0.67,P〈0.01）。结论子痫前期患者胎盘组织中的MIF的过度表达,可上调血浆中炎性标志物CRP的水平,引起血管内皮损伤,从而参与子痫前期的发病。     

Serum adiponectin, leptin and soluble leptin receptor in pre-eclampsia.

OBJECTIVES: To delineate the changes in serum levels of adiponectin, leptin and soluble leptin receptor, and in the free leptin index in women with pre-eclampsia. METHODS: Blood samples were collected from 38 pregnant women with pre-eclampsia and 42 normotensive pregnant women as controls. Serum concentrations of adiponectin, leptin and soluble leptin receptor were determined by enzyme-link immunosorbent assay and the free leptin index was calculated as the ratio of serum leptin to soluble leptin receptor for each sample. RESULTS: No significant differences were observed between the groups regarding maternal age, gestational age and body mass index. Women with pre-eclampsia had significantly higher levels of serum adiponectin and leptin, and a higher free leptin index than controls (P<0.01, P<0.001 and P<0.001, respectively). There were no significant differences between the two groups in serum levels of soluble leptin receptor (P>0.05). CONCLUSIONS: The study demonstrated elevated serum levels of adiponectin and leptin as well as a higher free leptin index in women with pre-eclampsia, suggesting these as important factors contributing to this complication of pregnancy.