ABSTRACT
Placental and maternal-fetal circulation Doppler ultrasound are the main noninvasive means for maternal-fetal monitoring. However, Doppler studies on placental abnormalities are not well studied yet. Doppler monitoring of the maternal-fetal circulation, involving uterine arteries, umbilical arteries, and fetal vessels, is still used to screen diseases related to placental dysfunction (such as preeclampsia and fetal growth restriction) and to guide clinical management. This article reviews the advances in the clinical application of placental and maternal-fetal circulation Doppler in obstetrics to optimize the clinical management of disorders associated with abnormal placental structure and function.
ABSTRACT
Placenta-mediated pregnancy complication (PMPC), including preeclampsia, fetal growth restriction and recurrent pregnancy loss, is caused by inadequate trophoblast invasion and abnormal remodeling of maternal spiral arteries in early pregnancy, resulting in adverse perinatal outcomes and affecting the long-term maternal and child health. However, the molecular mechanisms of PMPC remain unclear. Endocrine gland-derived vascular endothelial growth factor (EG-VEGF) is highly expressed in human placenta and plays an important role in the development of a normal placenta through promoting placental angiogenesis and inhibiting trophoblast migration and invasion. EG-VEGF dysregulation is closely related to the pathogenesis of PMPC. This review described recent advances in EG-VEGF for better understanding of the underlying mechanism of PMPC and providing a potential biomarker for early diagnosis of PMPC.
ABSTRACT
Placenta-mediated pregnancy complication (PMPC), including preeclampsia, fetal growth restriction and recurrent pregnancy loss, is caused by inadequate trophoblast invasion and abnormal remodeling of maternal spiral arteries in early pregnancy, resulting in adverse perinatal outcomes and affecting the long-term maternal and child health. However, the molecular mechanisms of PMPC remain unclear. Endocrine gland-derived vascular endothelial growth factor (EG-VEGF) is highly expressed in human placenta and plays an important role in the development of a normal placenta through promoting placental angiogenesis and inhibiting trophoblast migration and invasion. EG-VEGF dysregulation is closely related to the pathogenesis of PMPC. This review described recent advances in EG-VEGF for better understanding of the underlying mechanism of PMPC and providing a potential biomarker for early diagnosis of PMPC.
ABSTRACT
Objective Study the effects of early overfeeding in the adult offspring of mother with severely hyperglycaemia in pregnancy to islet development and insulin resistance. Methods Thirty healthy female Wistar rats were mated with 10 male Wistar rats and the morning on which sperm were found in three different visual fields of the vaginal smear was designated pregnancy day 1. The pregnant rats were intraperitoneally administered with Streptozotocin (STZ, 50 mg/L) on 5th day of pregnancy, and blood glucose exceeded 20 mmol/L to induce severely gestational diabetes mellitus (SDM) model. The pregnant Wistar rats were assigned to two experimental groups: SDM (n = 16) and control (n = 8). Litter size reduction in the lactation period induced early postnatal overfeeding model. Offspring were divided into three groups according to the level of blood glucose in pregnancy and feeding patterns in lactation: ( 1 ) control group (CG):euglycemia in pregnancy, eight pups in lactation;(2) severely gestational diabetes mellitusnormal feeding (SDM-N):severely gestational diabetes mellitus, eight pups in lactation; (3) severely gestational diabetes mellitus-overfeeding (SDM-O): severely gestational diabetes mellitus, four pups lactation. At the end of the lactation period, all pups were fed standard laboratory chow adlibitum until the date of the experiments. Offspring body weight was measured weekly after ablactation. Serum insulin was measured by enzyme-linked immunosorbent assay (ELISA) and pancreatic islet morphology was analyzed by immunohistochemistry (IHC) in all three groups at 26 weeks of age. Results (1) Blood glucose of pregnant Wistar rats: SDM (28.3 ±5.1 ) mmol/L was statistically higher than control (6.3 ± 1.4) mmol/L ( P ＜ 0.05 ). (2) Growth rates of body weight in 3 - 7 weeks and 3 - 9 weeks: SDM-N: (4. 6 ± 1.3) % and (6.8±2.5)%, SDM-O:(3.2±0.7)% and(4.6±1.2)%,CG:(2.9 ±0.6)% and(4.1 ±0.8)%.The growth rates of body weight in SDM-N and SDM-O were both significantly higher than those in CG ( P ＜0.05 ). (3) Body weight at 26 weeks: CG: (486 ± 132) g, SDM-N: ( 387 ± 115 ) g, SDM-O: ( 382 ± 122) g.There was no statistical difference among the three groups (P ＞0.05). (4) Fasting plasma glucose ( FPG),fasting insulin (FINS), homeostasis model of insulin resistance (HOMA-IR) and insulin sensitivity index (ISI): at 26 weeks, the SDM-offspring has nomal FPG, but more insulin was needed to keep it normal. The insulin level of SDM-O[ ( 12.6 ± 3.3) mU/L ] was statistically higher than those of SDM-N [ ( 10.9 ± 3.3 )mU/L] and CG [ ( 8.6 ± 0.8 ) mU/L ] ( P ＜ 0.05 ). The ISI of SDM-O ( 0.020 ± 0.006 ) was significantly smaller than its HOMA-IR(2.40 ±0.62,P ＜0.05). (5)The morphological change of pancreatic islet: The islets of CG and SDM-N were round or ellipse and have clear boundary between endocrine and exocrine parts and the β cells distributed equally. However, SDM-O islets were not of uniform size and most of islets were hyperplasia and hypertrophy. (6) Relative β cell area of pancreas, β-cell area and islet size: SDM-O:(1.81 ±0.31)%, (57.1 ±3.2)% and(39 067 ±3308)μm2; SDM-N:(1.34 ±0.43)%,(60.9 ±0.6)% and ( 30 570 ± 4824 ) μm2; CG: ( 1.11 ± 0.26 )%, ( 63.7 ± 2.7 )% and ( 26 443 ± 4431 ) μm2.SDM-O has significantly increasing β-cell mass, hypertrophic islet size and slightly decreasing β-cell percentage compared with other two groups (P ＜ 0.05 ). Conclusions The exposure of severely hyperglycemia in pregnancy induces low weight infant and postnatal catch-up growth leading to the possibility of insulin resislance (IR) in adult and early postnatal overfeeding will accelerate such course. Islet morphology of SDM-N has no significant change, indicating that maternal diabetes mainly affected β-cell function but not islet morphological features. SDM overfeeding results in early impairment of islet morphology and function, indicating that the compensation ability of islets has already been impaired and the risk of further development of impaired glucose tolerance (IGT) and diabetes. In conclusion, the nutritonal environment in early life ( duration of pregnancy and lactation) participate in the metabolic programming in adulthood.
ABSTRACT
Objective To explore the metabolic phenotype of the adult offspring rats with maternal severe hyperglycemia during pregnancy and overfeeding in early life. Methods The adult Wistar rats were administered intraperitoneally with 20% Streptozotocin (STZ, 50 mg/kg) on day 5 of pregnancy to induce severely gestational diabetes mellitus (SDM) model (blood glucose ≥20 mmol/L). Early postnatal overfeeding models were established through reduction of the number of newborn rats fed by one mother rat. Offsprings were divided into 3 groups according to maternal blood glucose level during the pregnancy and feeding patterns during the lactation period (1) control pups (CP) :maternal euglycemia was achieved during pregnancy and eight pups fed by one mother rat; (2)SDM-normal feeding group: SDM mothers and 8 pups fed by one mother rat;(3)SDM-overfeeding group:SDM mother and 4 pups fed by one mother rat. All pups were fed by standard laboratory chow adlibitum after weaning at 3 weeks of age. The body weight of all pups were measured weekly after weaning. At the age of 26 weeks, the systolic blood pressure (SBP), diastolic blood pressure (DBP) ,heart rate (HR) and metabolic markers, including fasting plasma glucose (FPG), fasting insulin (FINS), total triglyceride (TG), total cholesterol (TC), low density lipoprotein-cholestrol (LDL-C)and high density lipoprotein-cholestrol (HDL-C) were measured in all 3 groups. ANOVA and LSD test were applied in statistical analysis. Results The average plasma glucose level was significantly higher in the SDM mothers than in the controls [(28.34±5.14) mmol/L va (6.25±1.41) mmol/L,P＜0.05]. After weaning at 3 weeks, the weight of SDM-overfeeding group and SDM-normal feeding group was lighter than that of CP group [(43.63±4.83) g, (31.45±10.21) g vs (55.75±8.41) g,P＜0. 05], meanwhile, that of the SDM-overfeeding group were heavier than that of the SDM-normal feeding group (P＜0. 05). Pups in SDM-overfeeding group exhibited catch-up growth during the lactation period, and those in SDM-normal group showed catch-up growth at both lactation period and childhood. At 26 weeks of age, the systolic blood pressure and TG level of pups in SDM-normal feeding and overfeeding group were (153.31 ± 13.91) mm Hg and (147.21 ± 12.29) mm Hg, and (0. 73±0. 22) mmol/L and (0. 71±0.49) mmol/L, respectively, which were higher than those of the CP group [( 132.21 ± 11.26) mm Hg, and (0. 37 ± 0. 08) mmol/L, P＜0.05], but no significant difference was found between the two SDM groups (P＞0.05). There was no difference in FPG levels among the three groups, but the FINS level and HOMA-IR in the SDM-overfeeding group were higher than in the SDM normal feeding and CP group [( 12. 552 ± 3.260) mU/L vs (9.067 ± 1.782) mU/L and (8.590± 0.806) mU/L, 2.400± 0.624 vs 1.797 ± 0.508 and 1.729 ± 0.246; P＜0.05].Conclusions Fetal exposure to maternal severe hyperglycemia during pregnancy may lead to low birth weight infant who will exhibit postnatal catch-up growth. This may lead to the increased risk of metabolic syndrome in the offspings when they grow up, and this process would be accelerated by early overfeeding.