Background: Intra-uterine crowding(IUC) observed in hyperprolific sows impairs myofiber hyperplasia and overall fetal growth. Arginine supplementation(ARG) in gestation diets has been shown to positively affect litter...Background: Intra-uterine crowding(IUC) observed in hyperprolific sows impairs myofiber hyperplasia and overall fetal growth. Arginine supplementation(ARG) in gestation diets has been shown to positively affect litter and muscle development. The study objective was to assess whether the effect of ARG on offspring characteristics, with special emphasis on myofiber hyperplasia, differs under IUC conditions from these responses,because in that situation growth retardation is particularly prevalent due to reduced fetal nutrient supply.Unilateral oviduct ligation(OL) was used as a model for an uncrowded and hyperprolificacy(IN) as a model for a crowded intra-uterine environment.Methods: Five OL and five IN sows were fed a diet supplemented daily with either 43 g L-alanine(Ctrl) or 25 g L-arginine from d 14 to 28 of gestation in a cross-over design(two periods: 5^( th) and 6^( th) parity). At farrowing, two male and two female offspring, respectively, with a low and intermediate birth weight(BtW) were selected. After euthanization, the Semitendinosus muscle(STM) was removed and weighed, and the light and dark portions(STM_d and STM_l) were prepared for myofiber histochemistry using ATPase staining and the entire STM for gene expression analysis of myogenesis-related genes using RT-qPCR. In addition, various organs were removed and weighed. Data were analyzed using the MIXED model in SYSTAT.Results: No effect of either IUC or dietary treatment was found in litter characteristics. Offspring of ARG sows displayed a greater muscle area in STM(P < 0.01) as a result of the greater myofiber hyperplasia(P < 0.01). The increase was more distinct in the STM_l(P < 0.05) than in the STM_d(P = 0.131). Offspring of OL sows were heavier at birth(P < 0.01), had a heavier STM(P < 0.05), liver(P < 0.01) and kidney(P < 0.05), but when expressed relative to birth weight, these differences were absent. In addition, IUC had an effect(P < 0.05) on the expression of one of the myogenesis-related genes investigated.Conclusions: Independent fro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
Aim: Exposure to the ubiquitous endocrine disrupter Bisphenol A (BPA) has been associated, in pregnancy, with low birth weight. The aim of our study is the identification of the damage caused by Bisphenol A on placent...Aim: Exposure to the ubiquitous endocrine disrupter Bisphenol A (BPA) has been associated, in pregnancy, with low birth weight. The aim of our study is the identification of the damage caused by Bisphenol A on placental tissue through the evaluation of its effects on micro-vessel density and apoptosis. Methods: After fertilization, we exposed 3 female rats to oral BPA, by means of a free access to a beverage solution containing 100 μg/L of BPA. Three female rats were used as controls. Placentas underwent histological examination and immunohistochemistry for von Willebr and factor (F-VIII) and caspase-9. Results: Sixty-seven fetuses have been produced, 30 from control rats and 37 from exposed rats. Exposed fetuses showed a lower longitudinal/transverse diameter ratio than controls (2.57 ± 0.29 vs. 2.78 ± 0.38, p < 0.05). Also, exposed fetuses showed a significant reduction in the number of placental vessels per field (124.86 ± 19.15 vs. 143.54 ± 22.09, p < 0.05). On the other hand, apoptosis is not increased by exposure, as shown by caspase-9 levels. Conclusion: Exposure to BPA during pregnancy may affect placental vascularization, and this phenomenon may explain the lower birth weight reported. However, our results do not show the increase in apoptosis observed in vitro.展开更多
文摘Background: Intra-uterine crowding(IUC) observed in hyperprolific sows impairs myofiber hyperplasia and overall fetal growth. Arginine supplementation(ARG) in gestation diets has been shown to positively affect litter and muscle development. The study objective was to assess whether the effect of ARG on offspring characteristics, with special emphasis on myofiber hyperplasia, differs under IUC conditions from these responses,because in that situation growth retardation is particularly prevalent due to reduced fetal nutrient supply.Unilateral oviduct ligation(OL) was used as a model for an uncrowded and hyperprolificacy(IN) as a model for a crowded intra-uterine environment.Methods: Five OL and five IN sows were fed a diet supplemented daily with either 43 g L-alanine(Ctrl) or 25 g L-arginine from d 14 to 28 of gestation in a cross-over design(two periods: 5^( th) and 6^( th) parity). At farrowing, two male and two female offspring, respectively, with a low and intermediate birth weight(BtW) were selected. After euthanization, the Semitendinosus muscle(STM) was removed and weighed, and the light and dark portions(STM_d and STM_l) were prepared for myofiber histochemistry using ATPase staining and the entire STM for gene expression analysis of myogenesis-related genes using RT-qPCR. In addition, various organs were removed and weighed. Data were analyzed using the MIXED model in SYSTAT.Results: No effect of either IUC or dietary treatment was found in litter characteristics. Offspring of ARG sows displayed a greater muscle area in STM(P < 0.01) as a result of the greater myofiber hyperplasia(P < 0.01). The increase was more distinct in the STM_l(P < 0.05) than in the STM_d(P = 0.131). Offspring of OL sows were heavier at birth(P < 0.01), had a heavier STM(P < 0.05), liver(P < 0.01) and kidney(P < 0.05), but when expressed relative to birth weight, these differences were absent. In addition, IUC had an effect(P < 0.05) on the expression of one of the myogenesis-related genes investigated.Conclusions: Independent fro
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。
文摘Aim: Exposure to the ubiquitous endocrine disrupter Bisphenol A (BPA) has been associated, in pregnancy, with low birth weight. The aim of our study is the identification of the damage caused by Bisphenol A on placental tissue through the evaluation of its effects on micro-vessel density and apoptosis. Methods: After fertilization, we exposed 3 female rats to oral BPA, by means of a free access to a beverage solution containing 100 μg/L of BPA. Three female rats were used as controls. Placentas underwent histological examination and immunohistochemistry for von Willebr and factor (F-VIII) and caspase-9. Results: Sixty-seven fetuses have been produced, 30 from control rats and 37 from exposed rats. Exposed fetuses showed a lower longitudinal/transverse diameter ratio than controls (2.57 ± 0.29 vs. 2.78 ± 0.38, p < 0.05). Also, exposed fetuses showed a significant reduction in the number of placental vessels per field (124.86 ± 19.15 vs. 143.54 ± 22.09, p < 0.05). On the other hand, apoptosis is not increased by exposure, as shown by caspase-9 levels. Conclusion: Exposure to BPA during pregnancy may affect placental vascularization, and this phenomenon may explain the lower birth weight reported. However, our results do not show the increase in apoptosis observed in vitro.
