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

Bar, Jacob; Weiner, Eran; Levy, Michal; Gilboa, Y.

doi:10.1016/j.ajogmf.2021.100473

Cited by 12 publications

(7 citation statements)

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“…[ 40 ] Such alterations are beneficial if the undernutrition persists after birth but may predispose the individual to obesity and impaired glucose tolerance if conditions improve. [ 41 ] Therefore, long-term monitoring of insulin sensitivity and blood glucose levels in LBW infants is extremely significant. In the meantime, healthy nutritional habits during pregnancy should be strongly emphasized before pregnancy to ensure that the fetus receives proper nutrition from the first moment of the mother’s pregnancy.…”

Section: Discussionmentioning

confidence: 99%

Network exploration of gene signatures underlying low birth weight induced metabolic alterations

et al. 2022

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Background: This study explored underlying gene signatures of low birth weight (LBW) by analyzing differentially expressed genes (DEGs) between LBW and normal birth weight (NBW) subjects.Methods: Subjects with different birth weight was collected from GEO database. P < .05 and | logFC | ≥ 1.0 were used for screening DEGs. David (2021 Update) was used to perform GO annotation and KEGG signaling pathway enrichment analysis. The protein-protein interaction network of DEGs was constructed using the STRING database, in which hub genes were mined through Cytoscape software.Results: A total of 326 DEGs were identified, including 287 up-regulated genes and 39 down-regulated genes. The GO biological processes enriched by DEGs mainly involved epidermal growth, keratinization and intermediate fibrous tissue. The DEGs were significantly enriched in intracellular insoluble membranes, desmosomes and extracellular space. Their molecular functions mainly focused on structural molecular activity, structural components of epidermis and structural components of cytoskeleton. PI3K/ AKT signaling pathway and tight junction were highlighted as critical pathways enriched by DEGs. Ten hub genes which included KRT14, EGF, DSP, DSG1, KRT16, KRT6A, EPCAM, SPRR1B, PKP1, and PPL were identified from the constructed proteinprotein interaction network. Conclusion:A total of 326 DEGs and 10 hub genes were identified as candidates for metabolic disorders in LBW individuals. Our results indicated PI3K/AKT signaling pathway as an intrauterine adaptive mechanism for LBW individuals. We observed activated PI3K/AKT pathway in LBW individuals, which would promote growth and development at the early stage of life, but adversely introduce extra metabolic stress and thereby potentially induce metabolic disorders in adulthood.Abbreviations: BP = biological process, CC = cellular component, DAVID = database for annotation, visualization and integrated discovery, DEGs = differentially expressed genes, GEO = gene expression omnibus, GO = gene ontology, KEGG = kyoto encyclopedia of genes and genomes, LBW = low birth weight, MF = molecular function, PPI = protein-protein interaction.

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Section: Discussionmentioning

confidence: 99%

Network exploration of gene signatures underlying low birth weight induced metabolic alterations

et al. 2022

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“… 5 Animal models show that LBW is associated with insulin resistance and adiposity. 6–8 There are epigenetic speculations such as fetal insulin and the thrifty phenotype hypothesis for LBW inducing an imbalance in glucose and lipid homeostasis in adulthood, 9 , 10 but the specific molecular mechanism remains ambiguous. This limits the control and prevention of susceptibility to insulin resistance in LBW populations.…”

Section: Introductionmentioning

confidence: 99%

Adipose Dysfunction in Adulthood Insulin Resistance of Low-Birth Weight Mice: A Proteomics Study

Wang

Lin-de

Yang

et al. 2022

DMSO

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Purpose To investigate changes in the protein expression profile of white adipose tissue in low-birth weight (LBW) mice with high-fat diets using tandem mass tag (TMT) and liquid chromatography-mass spectrometry (LC-MS/MS) and parallel reaction monitoring (PRM). Methods Institute of Cancer Research (ICR) mice were used to establish an LBW model using malnutrition during pregnancy. Male pups were randomly selected from LBW and normal-birth weight (NBW) offspring, then all given a high-fat diet. Blood glucose, serum insulin, total cholesterol (TC) and triglyceride (TG) levels were measured. The weight ratio of liver, muscle, and adiposity index were calculated. Hematoxylin and eosin staining was used to visualize adipose tissue morphology. Oil red O staining of liver and TG content of muscle were used to determine ectopic lipid deposition. TMT combined with LC-MS/MS was used to analyze protein expression in white adipose tissue. PRM and Western blot were used to verify the expression of CD36, SCD1, PCK1 and PPARγ. Results Compared with NBW mice, fasting blood glucose, insulin and HOMA-IR significantly increased in LBW mice, indicating insulin resistance and impaired glucose regulation; TC, TG, adipocyte size, and adiposity index were increased in LBW mice, suggesting obesity and disorder of lipid metabolism. We observed ectopic lipid deposition in liver and muscle. There were 996 differentially expressed proteins (DEPs) in the LBW/NBW groups. Peroxisome proliferator-activated receptor (PPAR) was a relatively important signaling pathway regulating metabolic process in functional enrichment analysis of DEPs. Up-regulated expression of CD36, SCD1, and PCK1 in the adipose tissue of LBW mice was observed through PPAR pathways cluster analysis. And PRM and Western blot assay validated the proteomics findings. Conclusion When exposed to high-fat diets, LBW mice exhibited insulin resistance and disorder of lipid metabolism compared with NBW mice. The expression of PPARγ was elevated, as well as upstream CD36, downstream SCD1 and PCK1 of the PPARγ in the adipose tissue of LBW mice. It was suggested that the activation in CD36/PPARγ/SCD1 and CD36/PPARγ/PCK1 pathways may induce adipose dysfunction, thereby increasing susceptibility to insulin resistance.

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“…Fetal growth restriction (FGR) is one of the most common complications in the perinatal stage, and its diagnostic criteria are the failures of a fetus to achieve its due growth potential at a gestational age below the 10th percentile of the mean for that fetus of the same sex, or below 2,500 g after 37 weeks of gestation [ 1 , 2 ]. Based on the different pathogenic causes, FGR has been clinically classified into two categories, namely, FGR of definite etiology due to maternal primary disease and pregnancy comorbidities and FGR of unknown etiology, also known as idiopathic FGR (IFGR), which accounts for about 40% of the total incidence of FGR [ 3 – 5 ].…”

Section: Introductionmentioning

confidence: 99%

Correlation between Parturients’ Uterine Artery Blood Flow Spectra in the First and Second Trimesters of Pregnancy and Fetal Growth Restriction

et al. 2021

Journal of Healthcare Engineering

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Objective. To explore the correlation between parturients’ uterine artery blood flow spectra in the first and second trimesters of pregnancy and fetal growth restriction (FGR). Methods. The data of parturients treated in our hospital from February 2018 to February 2020 were retrospectively analyzed, 50 parturients with FGR were selected as the FGR group, and other 50 healthy cases were selected as the control group. In the first trimester (11-12 weeks of gestation) and the second trimester of pregnancy (13–24 weeks of gestation), the parturients of the two groups accepted the color Doppler ultrasonography (CDS), their hemodynamics indicators of uterine artery were recorded, and the correlation between their uterine artery blood flow spectra in the two periods and FGR was analyzed with the Receiver Operating Characteristic (ROC) curve. Results. No statistical differences in the parturients’ general information including age, gestational weeks, gravidity, and parity between the two groups were observed ( P > 0.05); the newborn’s body weight, Apgar scores, number of preterm infants, and the number of infants transferring to the neonatal intensive care unit (NICU) were significantly different between the two groups ( P < 0.05); in the first and second trimesters of pregnancy, the uterine artery pulsatility index (UtA-PI), uterine artery resistance index (UtA-RI), maximal systolic flow velocity, and systolic/diastolic (UtA-S/D) ratio were significantly higher in the FGR group than in the control group ( P < 0.05), and the time-averaged maximal velocity (TAMX) was significantly lower in the FGR group than in the control group ( P < 0.001); in early pregnancy, the incidence of early diastolic notch at bilateral uterine arteries between the two groups was not significantly different ( P > 0.05), and the unilateral and total incidence in the first trimester as well as the unilateral, bilateral, and total incidence in the second trimester were significantly higher in the FGR group than in the control group ( P < 0.05); in the first trimester, the sensitivity of detecting FGR with a uterine artery blood flow spectrum was 0.820, AUC (95% CI) = 0.840 (0.757–0.923), and in the second trimester, it was 0.860, AUC (95% CI) = 0.900 (0.832–0.968). Conclusion. There is a correlation between uterine artery blood flow spectra in the first and second trimesters of pregnancy and FGR, and the sensitivity of spectrum in the first trimester is higher than that in the second trimester, presenting a better clinical application value.

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

Cited by 12 publications

References 110 publications

Network exploration of gene signatures underlying low birth weight induced metabolic alterations

Network exploration of gene signatures underlying low birth weight induced metabolic alterations

Adipose Dysfunction in Adulthood Insulin Resistance of Low-Birth Weight Mice: A Proteomics Study

Correlation between Parturients’ Uterine Artery Blood Flow Spectra in the First and Second Trimesters of Pregnancy and Fetal Growth Restriction

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