scholarly journals Kajian Pustaka: Kadar Brain Derived Neurotrophic Factor Mempengaruhi Berat Badan Lahir pada Bayi

2019 ◽  
Vol 19 (1) ◽  
pp. 152
Author(s):  
Yessi Ardiani ◽  
Defrin Defrin ◽  
Husna Yetti

Brain Derived Neurotrhophic Factor (BDNF) is one of the proteins needed for the growth of neurons. During its development period BDNF plays a role in nerve growth, differentiation, repair, and survival of nerve cells. In addition, researchers from certain groups found that BDNF also had an important role during the implantation period, placental development and development of fetal growth. BDNF is known to have an important role in regulating angiogenesis needed for placental development. Because of this role, BDNF deficiency will cause disruption in placental growth which will eventually cause fetal growth disorders or Intrauterine growth restriction (IUGR). In recent years studies have shown that neurotrophins play an important role in the regulation of placental development and fetal growth. BDNF has been found to be expressed in large amounts in blastocysts which indicate the potential role of BDNF in implantation and development of the placenta. BDNF is also produced in the muscle tissue of one of them in the uterus precisely in the endometrium and myometrium. The discovery of the role of BDNF, is expected to be used as an indicator to assess the occurrence of growth disorders in the fetus as well as additional information about the etiology and pathophysiology of IUGR. Keywords: BDNF; IUGR; Neurotrophin

2007 ◽  
Vol 196 (1) ◽  
pp. 70.e1-70.e6 ◽  
Author(s):  
Cathal McCarthy ◽  
Finbarr E. Cotter ◽  
Suzanne McElwaine ◽  
Anne Twomey ◽  
Eoghan E. Mooney ◽  
...  

2017 ◽  
Vol 29 (6) ◽  
pp. 1239 ◽  
Author(s):  
Jorge López-Tello ◽  
María Arias-Álvarez ◽  
Maria-Ángeles Jiménez-Martínez ◽  
Alicia Barbero-Fernández ◽  
Rosa María García-García ◽  
...  

The present study evaluated the effectiveness of sildenafil citrate (SC) to improve placental and fetal growth in a diet-induced rabbit model of intrauterine growth restriction (IUGR). Pregnant rabbits were fed either ad libitum (Group C) or restricted to 50% of dietary requirements (Group R) or restricted and treated with SC (Group SC). The treatment with SC improved placental development by increasing vascularity and vessel hypertrophy in the decidua. The assessment of feto–placental haemodynamics showed higher resistance and pulsatility indices at the middle cerebral artery (MCA) in fetuses treated with SC when compared with Group R, which had increased systolic peak and time-averaged mean velocities at the MCA. Furthermore, fetuses in the SC group had significantly higher biparietal and thoracic diameters and longer crown–rump lengths than fetuses in Group R. Hence, the SC group had a reduced IUGR rate and a higher kit size at birth compared with Group R. In conclusion, SC may provide potential benefits in pregnancies with placental insufficiency and IUGR, partially counteracting the negative effects of food restriction on placental development and fetal growth. However, the present study also found evidence of a possible blood overflow in the brain that warrants further investigation.


2018 ◽  
Vol 60 (4) ◽  
pp. R201-R212 ◽  
Author(s):  
Jonathan Pham ◽  
Kanaga Arul Nambi Rajan ◽  
Ping Li ◽  
Mana M Parast

Placental development is important for proper in utero growth and development of the fetus, as well as maternal well-being during pregnancy. Abnormal differentiation of placental epithelial cells, called trophoblast, is at the root of multiple pregnancy complications, including miscarriage, the maternal hypertensive disorder preeclampsia and intrauterine growth restriction. The ligand-activated nuclear receptor, PPARγ, and nutrient sensor, Sirtuin-1, both play a role in numerous pathways important to cell survival and differentiation, metabolism and inflammation. However, each has also been identified as a key player in trophoblast differentiation and placental development. This review details these studies, and also describes how various stressors, including hypoxia and inflammation, alter the expression or activity of PPARγ and Sirtuin-1, thereby contributing to placenta-based pregnancy complications.


1995 ◽  
Vol 7 (6) ◽  
pp. 1457 ◽  
Author(s):  
E Alsat ◽  
C Marcotty ◽  
R Gabriel ◽  
A Igout ◽  
F Frankenne ◽  
...  

Consideration of the abnormal regulation of fetal growth leading to intrauterine growth retardation must take account of the fundamental differences between the regulation of growth before and after birth. The significance of endocrine regulators of growth differs greatly in utero. During the first trimester of pregnancy, embryonic growth might be controlled at the level of the individual organs by nutrient supply and by locally active growth factors. Later, fetal growth depends essentially upon materno-placental cooperation in delivering nutrients to the fetus. Therefore the major role of hormones in fetal growth is to mediate utilization of available substrate. Fetal growth seems to be regulated by fetal insulin, IGF-1 and certainly IGF-2, while growth hormone has only a secondary role to play. In late gestation, placental size and fetal growth rate are well correlated, pointing to a key role of the placenta in the regulation of fetal growth. It is therefore of importance to understand the molecular mechanisms involved in regulating placental development and endocrine functions. TGF alpha and EGF might play a major role as suggested by the modulation of their receptors with placental development, and by the specific alterations of epidermal growth factor receptors in intrauterine growth retardation. In addition, human placenta secretes specifically placental growth hormone. The concentration of placental growth hormone is significantly decreased in sera of pregnant women bearing a fetus with intrauterine growth retardation.


2005 ◽  
Vol 12 (3) ◽  
pp. 195-197 ◽  
Author(s):  
Ariadne Malamitsi-Puchner ◽  
Theodora Boutsikou ◽  
Emmanuel Economou ◽  
Evangelos Makrakis ◽  
Zoe Iliodromiti ◽  
...  

2007 ◽  
Vol 92 (7) ◽  
pp. 2758-2763 ◽  
Author(s):  
Rikke Beck Jensen ◽  
Signe Vielwerth ◽  
Torben Larsen ◽  
Gorm Greisen ◽  
Henrik Leffers ◽  
...  

Abstract Context: A common polymorphism in the GH receptor (GHR) gene has been linked to increased growth response in GH-treated patients. No former study has focused on the association to prenatal growth. Objective: The aim of the study was to evaluate the association between the d3-GHR isoforms and spontaneous pre- and postnatal growth. Design: A prospective study was conducted on third-trimester fetal growth velocity (FGV), birth weight, birth length, and postnatal growth. Setting: The study was conducted at Copenhagen University Hospital. Participants: A total of 115 healthy adolescents were divided into those born small for gestational age (SGA) and appropriate for gestational age with or without intrauterine growth restriction. Main Outcome Measures: FGV was measured by serial ultrasonography, birth weight, birth length, and adolescent height. Isoforms of the d3-GHR gene (fl/fl, d3/fl, and d3/d3) were determined. Results: The prevalence of the d3-GHR isoforms was 50% but differed among the groups (P = 0.006), with a high prevalence (88%) in the group born SGA with verified intrauterine growth restriction. The d3-GRH allele were associated with decreased third-trimester FGV (P = 0.05) in SGA subjects. In the entire cohort, carriers of the d3-GHR allele had a significantly increased height (−0.10 vs. 0.34 sd score; P = 0.017) and change in height from birth to adolescence compared with carriers of the full-length GHR allele (0.57 vs. −0.02 sd score; P = 0.005). Conclusions: This study showed an increased spontaneous postnatal growth velocity in the carriers of the d3-GHR allele. Interestingly, we found the opposite effect on prenatal growth in the SGA group, with a decreased FGV in carriers of the d3-GHR allele.


Author(s):  
Ying-xue Ding ◽  
Hong Cui

Abstract Brain injury is a serious complication of intrauterine growth restriction (IUGR), but the exact mechanism remains unclear. While glucocorticoids (GCs) play an important role in intrauterine growth and development, GCs also have a damaging effect on microvascular endothelial cells. Moreover, intrauterine adverse environments lead to fetal growth restriction and the hypothalamus-pituitary-adrenal (HPA) axis resetting. In addition, chronic stress can cause a decrease in the number and volume of astrocytes in the hippocampus and glial cells play an important role in neuronal differentiation. Therefore, it is speculated that the effect of GCs on cerebral neurovascular units under chronic intrauterine stimulation is an important mechanism leading to brain injury in infants with growth restrictions.


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