The Role of Leptin in Fetal Growth during Pre-Eclampsia

Knegt, Victoria Elizabeth de; Hedley, Paula L.; Kanters, Jørgen K.; Thagaard, Ida Näslund; Krebs, Lone; Christiansen, Michael; Lausten-Thomsen, Ulrik

doi:10.3390/ijms22094569

Cited by 38 publications

(31 citation statements)

References 118 publications

(285 reference statements)

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“…IUGR, due to uteroplacental insufficiency, results in a nephron deficiency and glomerular hypertrophy in both male and female rats [ 72 ]. Human studies appear to support these data because infants with SGA, which is often associated with placental insufficiency, have an increased risk of end-stage kidney disease compared to controls [ 73 ].…”

Section: Consequences For Offspringmentioning

confidence: 99%

Preeclampsia and Cardiovascular Risk for Offspring

Wojczakowski

Kimber-Trojnar

Dziwisz

et al. 2021

JCM

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There is growing evidence of long-term cardiovascular sequelae in children after in utero exposure to preeclampsia. Maternal hypertension and/or placental ischaemia during pregnancy increase the risk of hypertension, stroke, diabetes, and cardiovascular disease (CVD) in the offspring later in life. The mechanisms associated with CVD seem to be a combination of genetic, molecular, and environmental factors which can be defined as fetal and postnatal programming. The aim of this paper is to discuss the relationship between pregnancy complicated by preeclampsia and possibility of CVD in the offspring. Unfortunately, due to its multifactorial nature, a clear dependency mechanism between preeclampsia and CVD is difficult to establish.

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Section: Consequences For Offspringmentioning

confidence: 99%

Preeclampsia and Cardiovascular Risk for Offspring

Wojczakowski

Kimber-Trojnar

Dziwisz

et al. 2021

JCM

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“… 45 , 46 LEP encodes leptin, which is a hormone released by the placenta and is important in fetal growth throughout the entirety of pregnancy. 47 LEP up-regulation in IUGR placentas was reported in another 3 studies. 48 - 50 Leptin is crucial in placental development and function.…”

Section: Discussionmentioning

confidence: 71%

Bioinformatics Analysis Identifies Potential Related Genes in the Pathogenesis of Intrauterine Fetal Growth Retardation

Xiao

Wang

Fan

2022

Evol Bioinform Online

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Background: Intrauterine growth retardation (IUGR) affects approximately 10% to 15% of all pregnancies worldwide. IUGR is not only associated with stillbirth and newborn death, but also the delay of cognition in childhood and the promotion of metabolic and vascular disorders in adulthood. Figuring out the mechanism of IUGR is rather meaningful and valuable. Methods: Datasets related to IUGR were searched in the Gene Expression Omnibus website. Principal component analysis (PCA) was used for normalization. Differential expressed genes (DEGs) were screened out using the ggpot2 tool. DEGs were used to conduct Gene Ontology (GO) terms, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways enrichment analyses, and protein-protein interaction (PPI) analysis. IUGR related genes were searched in the OMIM website to look for the intersection with the DEGs. The DEGs were analyzed for tissue-specific expression by the online resource BioGPS. The results were displayed through volcano map, Venn map, box plot, heat map, and GSEA enrichment plots drawn by R language packages. Results: Eleven DEGs were screened out of 2 datasets. One hundred ninety-five genes related to IUGR in OMIM were retrieved. EGR2 was the only intersection gene that was found in both groups. Genes associated with placental tissue expression include COL17A1, HSD11B1, and LGALS14. Molecular functions of the DEGs are related to the oxidoreductase activity. The following 4 signaling pathways, reactome signaling by interleukins, reactome collagen degradation, Naba secreted factors, and PID NFAT tfpathway, were enriched by GSEA. Two critical modules comprising 5 up-regulated genes (LEP, PRL, TAC3, MMP14, and ADAMTS4) and 4 down-regulated genes (TIMP4, FOS, CCK, and KISS1) were identified by PPI analysis. Finally, we identified 6 genes (PRL, LGALS14, EGR2, TAC3, LEP, and KISS1) that are potentially relevant to the pathophysiology of IUGR. Conclusion: The candidate down-regulated genes LGALS14 and KISS1, as well as the up-regulated genes PRL, EGR2, TAC3, and LEP, were found to be closely related to IUGR by bioinformatics analysis. These hub genes are related to hypoxia and oxidoreductase activities in placental development. We provide useful and novel information to explore the potential mechanism of IUGR and make efforts to the prevention of IUGR.

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“…Maternal plasma leptin concentration was associated with infants change in weight ( p = 0.017) and confirmed in the partial correlation when adjusting for time and neonate type (−0.27). Previous studies reported no association between maternal leptin concentration and birthweight/weight change [ 6 , 20 ]; or higher incidence of IUGR neonate in pre-eclamptic pregnancy, if maternal serum leptin levels were elevated [ 21 ]. Moreover, a significant rate of low-birth-weight infants in non-diabetic mothers with high leptin plasma concentration was reported [ 22 , 23 ].…”

Section: Discussionmentioning

confidence: 99%

Leptin Levels of the Perinatal Period Shape Offspring’s Weight Trajectories through the First Year of Age

et al. 2022

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Background: Leptin is a hormone regulating lifetime energy homeostasis and metabolism and its concentration is important starting from prenatal life. We aimed to investigate the association of perinatal leptin concentrations with growth trajectories during the first year of life. Methods: Prospective, longitudinal study, measuring leptin concentration in maternal plasma before delivery, cord blood (CB), and mature breast milk and correlating their impact on neonate’s bodyweight from birth to 1 year of age, in 16 full-term (FT), 16 preterm (PT), and 13 intrauterine growth-restricted (IUGR) neonates. Results: Maternal leptin concentrations were highest in the PT group, followed by IUGR and FT, with no statistical differences among groups (p = 0.213). CB leptin concentrations were significantly higher in FT compared with PT and IUGR neonates (PT vs. FT; IUGR vs. FT: p < 0.001). Maternal milk leptin concentrations were low, with no difference among groups. Maternal leptin and milk concentrations were negatively associated with all the neonates’ weight changes (p = 0.017 and p = 0.006), while the association with CB leptin was not significant (p = 0.051). Considering each subgroup individually, statistical analysis confirmed the previous results in PT and IUGR infants, with the highest value in the PT subgroup. In addition, this group’s results negatively correlated with CB leptin (p = 0.026) and showed the largest % weight increase. Conclusions: Leptin might play a role in neonatal growth trajectories, characterized by an inverse correlation with maternal plasma and milk. PT infants showed the highest correlation with hormone levels, regardless of source, seeming the most affected group by leptin guidance. Low leptin levels appeared to contribute to critical neonates’ ability to recover a correct body weight at 1 year. An eventual non-physiological “catch-up growth” should be monitored, and leptin perinatal levels may be an indicative tool. Further investigations are needed to strengthen the results.

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The Role of Leptin in Fetal Growth during Pre-Eclampsia

Cited by 38 publications

References 118 publications

Preeclampsia and Cardiovascular Risk for Offspring

Preeclampsia and Cardiovascular Risk for Offspring

Bioinformatics Analysis Identifies Potential Related Genes in the Pathogenesis of Intrauterine Fetal Growth Retardation

Leptin Levels of the Perinatal Period Shape Offspring’s Weight Trajectories through the First Year of Age

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