Epigenetic Programming and Fetal Metabolic Programming

Zhu, Ziqiang; Cao, Fang; Li, Xiaozhong

doi:10.3389/fendo.2019.00764

Cited by 90 publications

(90 citation statements)

References 199 publications

(211 reference statements)

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“…Maternal pregestational-overweight is an independent factor linked with infant and adolescence overweight and abdominal obesity [4,5]. The "programming" hypothesis was advanced which suggests that exposure to suboptimal maternal conditions in the uterus, such as gestational diabetes mellitus (GDM), preeclampsia and obesity are risk factors promoting disease in the offspring because they disrupt homeostatic control of development [6,7]. This concept is gaining acceptance based on epidemiological studies and results obtained in animal models of obesity [8][9][10].…”

Section: Introductionmentioning

confidence: 99%

Maternal obesity alters C19MC microRNAs expression profile in fetal umbilical cord blood

Jia¹,

Wang²,

Quan³

et al. 2020

Nutr Metab (Lond)

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Background: To determine if overweight/obese pregnant women have altered microRNA expression patterns in fetal umbilical cord blood that may affect the development of offspring. Methods: Umbilical cord blood samples were obtained from the fetuses of 34 overweight/obese and 32 normalweight women after delivery. Next generation sequencing (NGS) analyzed their miRNA expression patterns. miRanda and TargetScan databases were used to predict the miRNAs' target genes followed by analyses of Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) to perform function grouping and pathway analyses. qRT-PCR verified the identity of differentially expressed miRNAs that were revealed in the NGS results. Results: There was a positive correlation between newborn body weight and pregestational BMI of pregnant individuals (r = 0.48, P < 0.001). One hundred and eight miRNAs were differentially expressed between the normal and overweight/obese groups, which target genes were enriched in the metabolic pathway. Five C19MC miRNAs (miR-516a-5p, miR-516b-5p, miR-520a-3p, miR-1323, miR-523-5p) were upregulated in the overweight/obese group. Target enrichment analysis suggests their involvement in post-embryonic development, lipid and glucose homeostasis, T cell differentiation and nervous system development. Conclusions: C19MC miRNA expression upregulation in the fetal circulation during the gestation of overweight/ obese pregnant women may contribute to altered multisystem metabolic pathway development in their offspring.

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Section: Introductionmentioning

confidence: 99%

Maternal obesity alters C19MC microRNAs expression profile in fetal umbilical cord blood

Jia¹,

Wang²,

Quan³

et al. 2020

Nutr Metab (Lond)

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“…It has been supported by significant decreasing of testosterone levels (median was 3.90 nmol/l apart 23.80 nmol/l, accordantly, p < 0.05, that may confirm substantial initial differences of placenta functioning under the conditions of different reproductive age with influence on the base enzymes of synthesis and/or metabolism It should be noted, that Glutathione content has decreased in both offspring groups under the influence of FPI. According to the recent trends, compensatory enzymes activation in offspring undergone different stress factors during pregnancy is linked to epigenetic activating of stress-reacting pathways that further may lead to the resources exhaustion and chronic inflammatory disease development [7,8]. On the other hand, the inhibition protecting systems components or different metabolic enzymes are often linked to protein molecules modifying during ontogenesis [9,10].…”

Section: Results and Their Discussionmentioning

confidence: 99%

“…Later, the epigenetic programming of gametes, embryonic cells and tissues and stem cells developing during critical «window» (sensitive period) of ontogenesis was linked to phenomenon mentioned above. During this sensitive period, adverse impact on mother's organism causes disturbances of pregnancy, regulates fetal growing and leads to disease developing in later life [7,8]. Epigenetic modifications, which represent an inheritance of gene expression without changes in sequence of DNA nucleotides, may be relatively stable during cells proliferation and, therefore, may persist over time.…”

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confidence: 99%

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Seliukova

Misyura

Boiko

et al. 2020

PEP

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The aim of this scientific work was to determine the influence of the experimental fetoplacental insufficiency on the both sex offspring oxidative status during puberty and to estimate the efficiency of base and complextherapy during pregnancy.Materials. The healthy, Vistar mature rat’s females of young (3–4 months) and mature (8–10 months)reproductive age have been used for both sex offspring obtaining. 8 groups for 7 pregnant females in eachhave been formed: Groups I and II — intact animals of young and mature reproductive age; Group III andIV — females with experimental Fetoplacental insufficiency (FPI) of young and mature reproductive age accordingly; Groups V and VI — young and mature animals with experimental FPI treated by pharmaceuticalcomposition which contains nontoxic active pharmaceutical ingredients of FPI basic therapeutic group — aminoacid (L-arginine), dicarbonic acid (succinic acid), vitamins (folic acid) and vasoactive drug (dipyridamole).Experimental animals have received treatment from 11 to 19 day of pregnancy. Groups VII and VIII — youngand mature animals with experimental FPI treated by drug of comparison — dipyridamole. The modeling ofFPI has been carried out by daily subcutaneous introduction of 50 % tetrachlormethane oil solution in dose of2 ml/kg of body weight from 12 to 18 day of pregnancy. Animals — offspring have been killed on the 50th day oflife (puberty period) by quick decapitation without general anesthesia to avoid negative effects on sex hormoneslevel and antioxidant enzymes systems.Results. The effect of experimental fetoplacental insufficiency in rats of young and mature reproductiveage on the oxidative status formation in offspring of both sexes during puberty was determined and the effectsof basic and complex therapy during pregnancy were evaluated. It was revealed that fetoplacental insufficiencyin the second half of pregnancy leads to the formation in offspring of both sexes, but more pronounced in maleoffspring, during the puberty, an altered pattern of the antioxidant system enzymatic activity, which is realizedin increased levels of both primary and final products of lipoperoxidation and may be the basis for further development of chronic diseases. More pronounced disorders were observed in the offspring of mothers of maturereproductive age, which may be due to the additional influence of involutive processes in the placenta. The useof a vasodilator drug alone and, more effectively in combination, significantly restored the studied parameters

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“…It has indeed been shown in other models of nutritional insult in pregnant mice (e.g. high-fat, methyl-deficient or low-protein diets) that induction of epigenetic marks in beta cells leads to altered function and diabetes risk later in life [ 47 , 48 ]. These epigenetic changes might be in part mediated through changes in maternal thyroid hormone secretion, since nutritional status is an important regulator of thyroid activity [ 49 ].…”

Section: Discussionmentioning

confidence: 99%

Maternal hypothyroidism in mice influences glucose metabolism in adult offspring

et al. 2020

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Aims/hypothesis During pregnancy, maternal metabolic disease and hormonal imbalance may alter fetal beta cell development and/or proliferation, thus leading to an increased risk for developing type 2 diabetes in adulthood. Although thyroid hormones play an important role in fetal endocrine pancreas development, the impact of maternal hypothyroidism on glucose homeostasis in adult offspring remains poorly understood. Methods We investigated this using a mouse model of hypothyroidism, induced by administration of an iodine-deficient diet supplemented with propylthiouracil during gestation. Results Here, we show that, when fed normal chow, adult mice born to hypothyroid mothers were more glucose-tolerant due to beta cell hyperproliferation (two- to threefold increase in Ki67-positive beta cells) and increased insulin sensitivity. However, following 8 weeks of high-fat feeding, these offspring gained 20% more body weight, became profoundly hyperinsulinaemic (with a 50% increase in fasting insulin concentration), insulin-resistant and glucose-intolerant compared with controls from euthyroid mothers. Furthermore, altered glucose metabolism was maintained in a second generation of animals. Conclusions/interpretation Therefore, gestational hypothyroidism induces long-term alterations in endocrine pancreas function, which may have implications for type 2 diabetes prevention in affected individuals.

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Epigenetic Programming and Fetal Metabolic Programming

Cited by 90 publications

References 199 publications

Maternal obesity alters C19MC microRNAs expression profile in fetal umbilical cord blood

Maternal obesity alters C19MC microRNAs expression profile in fetal umbilical cord blood

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Maternal hypothyroidism in mice influences glucose metabolism in adult offspring

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