Gestational diabetes mellitus(GDM)is a pregnancy-related complication characterized by abnormal glucose metabolism in pregnant women and has an important impact on fetal development.As a bridge between the mother and ...Gestational diabetes mellitus(GDM)is a pregnancy-related complication characterized by abnormal glucose metabolism in pregnant women and has an important impact on fetal development.As a bridge between the mother and the fetus,the placenta has nutrient transport functions,endocrine functions,etc.,and can regulate placental nutrient transport and fetal growth and development according to maternal metabolic status.Only by means of placental transmission can changes in maternal hyperglycemia affect the fetus.There are many reports on the placental pathophysiological changes associated with GDM,the impacts of GDM on the growth and development of offspring,and the prevalence of GDM in offspring after birth.Placental epigenetic changes in GDM are involved in the programming of fetal development and are involved in the pathogenesis of later chronic diseases.This paper summarizes the effects of changes in placental nutrient transport function and hormone secretion levels due to maternal hyperglycemia and hyperinsulinemia on the development of offspring as well as the participation of changes in placental epigenetic modifications due to maternal hyperglycemia in intrauterine fetal programming to promote a comprehensive understanding of the impacts of placental epigenetic modifications on the development of offspring from patients with GDM.展开更多
目的探讨抑制Hippo-YAP信号通路的激活是否能改善维生素D缺乏(vitamin D deficiency,VDD)所导致的胎盘及胚胎发育不良。方法按照体质量将4w龄SD雌性大鼠随机分为对照组(Ctrl)、VD缺乏组(VDD)、VD缺乏阴性对照组(VDD+vehicle)与VD缺乏抑...目的探讨抑制Hippo-YAP信号通路的激活是否能改善维生素D缺乏(vitamin D deficiency,VDD)所导致的胎盘及胚胎发育不良。方法按照体质量将4w龄SD雌性大鼠随机分为对照组(Ctrl)、VD缺乏组(VDD)、VD缺乏阴性对照组(VDD+vehicle)与VD缺乏抑制剂组(VDD+XMU-MP-1),Ctrl组采用标准饲料喂养,VDD组采用VD缺乏饲料喂养,喂养8 w后雌雄合笼。VDD+vehicle组与VDD+XMU-MP-1组在妊娠0-10 d(GD 0-10)进行腹腔注射。结果VD缺乏8 w后,与Ctrl组相比,VDD组血清25(OH)D水平均降低,且Ctrl组与VDD组、VDD+vehicle组间差异均有统计学差异(P<0.05);GD18时,与Ctrl组相比,VDD组血清25(OH)D水平略有降低。GD18时,与Ctrl组相比,VDD组、VDD+vehicle组(P<0.01)及VDD+XMU-MP-1组(P<0.01)胎盘25(OH)D水平均降低;与Ctrl组相比,其他三组胎盘1,25(OH)2D水平均有所降低,且Ctrl组与VDD+vehicle组、VDD+XMU-MP-1组均有统计学差异(P<0.01)。与Ctrl组相比,VDD组胎盘(P<0.01)、胚胎(P<0.05)重量明显下降,与VDD+vehicle组相比,VDD+XMU-MP-1组胎盘重量有所增加,组间有统计学差异(P<0.05),而胚胎重量略有增加;与Ctrl组相比,VDD组胎盘直径、胚胎冠臀长明显降低,且均有统计学差异(P<0.01),与VDD+vehicle组相比,VDD+XMU-MP-1组胎盘直径(P<0.05)、胚胎冠臀长(P<0.01)有所增加。结论维生素D缺乏对胚胎发育的损害作用涉及胎盘组织Hippo-YAP通路的激活,Hippo-YAP信号通路可能是预防维生素D缺乏所致不良妊娠结局的潜在靶点。展开更多
目的探究维生素D(vitaminD,VD)缺乏经Hippo-YAP信号通路抑制胎盘的发育,进而导致胎儿宫内生长受限的发生机制。方法按照体质量将4w龄SD雌性大鼠随机分为VD缺乏组(vitamin D deficiency,VDD)与对照组(CTRL),VDD组采用VD缺乏饲料喂养,CTR...目的探究维生素D(vitaminD,VD)缺乏经Hippo-YAP信号通路抑制胎盘的发育,进而导致胎儿宫内生长受限的发生机制。方法按照体质量将4w龄SD雌性大鼠随机分为VD缺乏组(vitamin D deficiency,VDD)与对照组(CTRL),VDD组采用VD缺乏饲料喂养,CTRL组采用标准饲料喂养,喂养8周后雌雄合笼。结果妊娠13d(GD13)与GD18时,VDD组孕鼠的血清25(OH)D浓度分别为(2.82±0.18)ng/ml和(14.67±7.92)ng/ml,对照组孕鼠的血清25(OH)D浓度分别为(36.58±10.58)ng/ml和(19.92±6.91)ng/ml,组间比较在GD13时有差异(P<0.0001)。GD13时,VDD组孕鼠的胚胎着床数(12.83±1.17)显著低于CTRL组的(15.83±1.47)(P<0.01);GD18时,VDD组孕鼠胚胎着床数(12.83±2.23),显著低于CTRL组的(15.67±1.03)(P<0.05),VDD组孕鼠的胎儿流产率也明显上升。GD18时,VDD组孕鼠的胎盘重量平均为(2.93±0.42)g,显著低于CTRL组的(6.38±0.48)g(P<0.0001);VDD组孕鼠的胎盘海绵体滋养层细胞面积为(11.63±0.03)%,显著小于CTRL组的(22.63±0.01)%(P<0.05);VDD组的活胎数,孕鼠孕期增重显著降低(P<0.01或P<0.0001),吸收胎数显著增加(P<0.05)。GD13时,与CTRL组相比,VDD组孕鼠胎盘组织中YAP1蛋白表达水平显著降低(P<0.01),P-YAP蛋白表达水平显著增高(P<0.001)。结论母体VD缺乏是导致妊娠后胚胎发育迟缓的重要原因,其机制可能涉及Hippo-YAP信号通路的激活,在孕前及孕期合理补充VD对胎儿健康具有重要意义。展开更多
文摘Gestational diabetes mellitus(GDM)is a pregnancy-related complication characterized by abnormal glucose metabolism in pregnant women and has an important impact on fetal development.As a bridge between the mother and the fetus,the placenta has nutrient transport functions,endocrine functions,etc.,and can regulate placental nutrient transport and fetal growth and development according to maternal metabolic status.Only by means of placental transmission can changes in maternal hyperglycemia affect the fetus.There are many reports on the placental pathophysiological changes associated with GDM,the impacts of GDM on the growth and development of offspring,and the prevalence of GDM in offspring after birth.Placental epigenetic changes in GDM are involved in the programming of fetal development and are involved in the pathogenesis of later chronic diseases.This paper summarizes the effects of changes in placental nutrient transport function and hormone secretion levels due to maternal hyperglycemia and hyperinsulinemia on the development of offspring as well as the participation of changes in placental epigenetic modifications due to maternal hyperglycemia in intrauterine fetal programming to promote a comprehensive understanding of the impacts of placental epigenetic modifications on the development of offspring from patients with GDM.
文摘目的探究维生素D(vitaminD,VD)缺乏经Hippo-YAP信号通路抑制胎盘的发育,进而导致胎儿宫内生长受限的发生机制。方法按照体质量将4w龄SD雌性大鼠随机分为VD缺乏组(vitamin D deficiency,VDD)与对照组(CTRL),VDD组采用VD缺乏饲料喂养,CTRL组采用标准饲料喂养,喂养8周后雌雄合笼。结果妊娠13d(GD13)与GD18时,VDD组孕鼠的血清25(OH)D浓度分别为(2.82±0.18)ng/ml和(14.67±7.92)ng/ml,对照组孕鼠的血清25(OH)D浓度分别为(36.58±10.58)ng/ml和(19.92±6.91)ng/ml,组间比较在GD13时有差异(P<0.0001)。GD13时,VDD组孕鼠的胚胎着床数(12.83±1.17)显著低于CTRL组的(15.83±1.47)(P<0.01);GD18时,VDD组孕鼠胚胎着床数(12.83±2.23),显著低于CTRL组的(15.67±1.03)(P<0.05),VDD组孕鼠的胎儿流产率也明显上升。GD18时,VDD组孕鼠的胎盘重量平均为(2.93±0.42)g,显著低于CTRL组的(6.38±0.48)g(P<0.0001);VDD组孕鼠的胎盘海绵体滋养层细胞面积为(11.63±0.03)%,显著小于CTRL组的(22.63±0.01)%(P<0.05);VDD组的活胎数,孕鼠孕期增重显著降低(P<0.01或P<0.0001),吸收胎数显著增加(P<0.05)。GD13时,与CTRL组相比,VDD组孕鼠胎盘组织中YAP1蛋白表达水平显著降低(P<0.01),P-YAP蛋白表达水平显著增高(P<0.001)。结论母体VD缺乏是导致妊娠后胚胎发育迟缓的重要原因,其机制可能涉及Hippo-YAP信号通路的激活,在孕前及孕期合理补充VD对胎儿健康具有重要意义。
