The thrifty phenotype hypothesis: The association between ultrasound and Doppler studies in fetal growth restriction and the development of adult disease

Author(s):  
Jacob Bar ◽  
Eran Weiner ◽  
Michal Levy ◽  
Yinon Gilboa
Author(s):  
Elizabeth Magalhães ◽  
Maria Méio ◽  
Maria Moreira

AbstractThe hypothesis of fetal origins to adult diseases proposes that metabolic chronic disorders, including cardiovascular diseases, diabetes, and hypertension originate in the developmental plasticity due to intrauterine insults. These processes involve an adaptative response by the fetus to changes in the environmental signals, which can promote the reset of hormones and of the metabolism to establish a “thrifty phenotype”. Metabolic alterations during intrauterine growth restriction can modify the fetal programming. The present nonsystematic review intended to summarize historical and current references that indicated that developmental origins of health and disease (DOHaD) occur as a consequence of altered maternal and fetal metabolic pathways. The purpose is to highlight the potential implications of growth factors and adipokines in “developmental programming”, which could interfere in the development by controlling fetal growth patterns. These changes affect the structure and the functional capacity of various organs, including the brain, the kidneys, and the pancreas. These investigations may improve the approach to optimizing antenatal as well as perinatal care aimed to protect newborns against long-term chronic diseases.


2017 ◽  
Vol 216 (1) ◽  
pp. S152
Author(s):  
Shannon L. Son ◽  
Diane Gumina ◽  
Mary Pinter ◽  
Allison Gillan ◽  
Darleen Cioffi-Ragan ◽  
...  

2021 ◽  
Vol 23 (1) ◽  
pp. 293
Author(s):  
Gabriela Loscalzo ◽  
Julia Scheel ◽  
José Santiago Ibañez Cabellos ◽  
Eva García-Lopez ◽  
Shailendra Gupta ◽  
...  

In a prospective study, 48 fetuses were evaluated with Doppler ultrasound after 34 weeks and classified, according to the cerebroplacental ratio (CPR) and estimated fetal weight (EFW), into fetuses with normal growth and fetuses with late-onset fetal growth restriction (LO-FGR). Overexpression of miRNAs from neonatal cord blood belonging to LO-FGR fetuses, was validated by real-time PCR. In addition, functional characterization of overexpressed miRNAs was performed by analyzing overrepresented pathways, gene ontologies, and prioritization of synergistically working miRNAs. Three miRNAs: miR-25-3p, miR-185-5p and miR-132-3p, were significantly overexpressed in cord blood of LO-FGR fetuses. Pathway and gene ontology analysis revealed over-representation of certain molecular pathways associated with cardiac development and neuron death. In addition, prioritization of synergistically working miRNAs highlighted the importance of miR-185-5p and miR-25-3p in cholesterol efflux and starvation responses associated with LO-FGR phenotypes. Evaluation of miR-25-3p; miR-132-3p and miR-185-5p might serve as molecular biomarkers for the diagnosis and management of LO-FGR; improving the understanding of its influence on adult disease.


Author(s):  
Yakubova D.I.

Objective of the study: Comprehensive assessment of risk factors, the implementation of which leads to FGR with early and late manifestation. To evaluate the results of the first prenatal screening: PAPP-A, B-hCG, made at 11-13 weeks. Materials and Methods: A retrospective study included 110 pregnant women. There were 48 pregnant women with early manifestation of fetal growth restriction, 62 pregnant women with late manifestation among them. Results of the study: The risk factors for the formation of the FGR are established. Statistically significant differences in the indicators between groups were not established in the analyses of structures of extragenital pathology. According to I prenatal screening, there were no statistical differences in levels (PAPP-A, b-hCG) in the early and late form of FGR.


2018 ◽  
pp. 184-195
Author(s):  
Minh Son Pham ◽  
Vu Quoc Huy Nguyen ◽  
Dinh Vinh Tran

Small for gestational age (SGA) and fetal growth restriction (FGR) is difficult to define exactly. In this pregnancy condition, the fetus does not reach its biological growth potential as a consequence of impaired placental function, which may be because of a variety of factors. Fetuses with FGR are at risk for perinatal morbidity and mortality, and poor long-term health outcomes, such as impaired neurological and cognitive development, and cardiovascular and endocrine diseases in adulthood. At present no gold standard for the diagnosis of SGA/FGR exists. The first aim of this review is to: summarize areas of consensus and controversy between recently published national guidelines on small for gestational age or fetal growth restriction; highlight any recent evidence that should be incorporated into existing guidelines. Another aim to summary a number of interventions which are being developed or coming through to clinical trial in an attempt to improve fetal growth in placental insufficiency. Key words: fetal growth restriction (FGR), Small for gestational age (SGA)


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