Comparison between placental gene expression of 11β‐hydroxysteroid dehydrogenases and infantile growth at 10 months of age

Muramatsu-Kato, Keiko; Itoh, Hiroaki; Kobayashi-Kohmura, Yukiko; Murakami, Hirotake; Uchida, Toshiyuki; Suzuki, Kazunao; Sato, Kazuhiro; Kanayama, Naohiro; Tsuchiya, Kenji J.; Takei, Nori

doi:10.1111/jog.12200

Cited by 11 publications

(14 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Both isoforms have been found relevant to childhood obesity (Ruan et al, 2014 ), the antecedent of MetS. In interaction with adiponectin, HSD11B1 determines the metabolic rate already in utero and postnatal development (Muramatsu-Kato et al, 2014 ), in a form of ontogenetic programming. HSD11B2 (16q22) protects cells from the growth-inhibiting and/or pro-apoptotic effects of cortisol, particularly during embryonic development.…”

Section: Genomic Foundation Of Basic Regulatory Mechanisms In Metsmentioning

confidence: 99%

Neuroendocrinological and Epigenetic Mechanisms Subserving Autonomic Imbalance and HPA Dysfunction in the Metabolic Syndrome

2016

View full text Add to dashboard Cite

Impact of environmental stress upon pathophysiology of the metabolic syndrome (MetS) has been substantiated by epidemiological, psychophysiological, and endocrinological studies. This review discusses recent advances in the understanding of causative roles of nutritional factors, sympathomedullo-adrenal (SMA) and hypothalamic-pituitary adrenocortical (HPA) axes, and adipose tissue chronic low-grade inflammation processes in MetS. Disturbances in the neuroendocrine systems for leptin, melanocortin, and neuropeptide Y (NPY)/agouti-related protein systems have been found resulting directly in MetS-like conditions. The review identifies candidate risk genes from factors shown critical for the functioning of each of these neuroendocrine signaling cascades. In its meta-analytic part, recent studies in epigenetic modification (histone methylation, acetylation, phosphorylation, ubiquitination) and posttranscriptional gene regulation by microRNAs are evaluated. Several studies suggest modification mechanisms of early life stress (ELS) and diet-induced obesity (DIO) programming in the hypothalamic regions with populations of POMC-expressing neurons. Epigenetic modifications were found in cortisol (here HSD11B1 expression), melanocortin, leptin, NPY, and adiponectin genes. With respect to adiposity genes, epigenetic modifications were documented for fat mass gene cluster APOA1/C3/A4/A5, and the lipolysis gene LIPE. With regard to inflammatory, immune and subcellular metabolism, PPARG, NKBF1, TNFA, TCF7C2, and those genes expressing cytochrome P450 family enzymes involved in steroidogenesis and in hepatic lipoproteins were documented for epigenetic modifications.

show abstract

Section: Genomic Foundation Of Basic Regulatory Mechanisms In Metsmentioning

confidence: 99%

Neuroendocrinological and Epigenetic Mechanisms Subserving Autonomic Imbalance and HPA Dysfunction in the Metabolic Syndrome

2016

View full text Add to dashboard Cite

show abstract

“…Hydroxysteroid dehydrogenases 11β control the passage of glucocorticoids from the mother to the fetus. In humans, placental expression of HSD11β1 is associated with birth weight [ 44 ]; placental HSD11βs expression is reduced in SGA neonates [ 45 ]. Impaired placental insulin signaling is associated with obesity, gestational diabetes mellitus, or intrauterine growth restriction (IUGR) [ 46 , 47 ].…”

Section: Discussionmentioning

confidence: 99%

Expression of epigenetic machinery genes is sensitive to maternal obesity and weight loss in relation to fetal growth in mice

et al. 2016

View full text Add to dashboard Cite

BackgroundMaternal obesity impacts fetal growth and pregnancy outcomes. To counteract the deleterious effects of obesity on fertility and pregnancy issue, preconceptional weight loss is recommended to obese women. Whether this weight loss is beneficial/detrimental for offspring remains poorly explored. Epigenetic mechanisms could be affected by maternal weight changes, perturbing expression of key developmental genes in the placenta or fetus. Our aim was to investigate the effects of chronic maternal obesity on feto-placental growth along with the underlying epigenetic mechanisms. We also tested whether preconceptional weight loss could alleviate these effects.ResultsFemale mice were fed either a control diet (CTRL group), a high-fat diet (obese (OB) group), or a high-fat diet switched to a control diet 2 months before conception (weight loss (WL) group). At mating, OB females presented an obese phenotype while WL females normalized metabolic parameters. At embryonic day 18.5 (E18.5), fetuses from OB females presented fetal growth restriction (FGR; −13 %) and 28 % of the fetuses were small for gestational age (SGA). Fetuses from WL females normalized this phenotype. The expression of 60 epigenetic machinery genes and 32 metabolic genes was measured in the fetal liver, placental labyrinth, and junctional zone. We revealed 23 genes altered by maternal weight trajectories in at least one of three tissues. The fetal liver and placental labyrinth were more responsive to maternal obesity than junctional zone. One third (18/60) of the epigenetic machinery genes were differentially expressed between at least two maternal groups. Interestingly, genes involved in the histone acetylation pathway were particularly altered (13/18). In OB group, lysine acetyltransferases and Bromodomain-containing protein 2 were upregulated, while most histone deacetylases were downregulated. In WL group, the expression of only a subset of these genes was normalized.ConclusionsThis study highlights the high sensitivity of the epigenetic machinery gene expression, and particularly the histone acetylation pathway, to maternal obesity. These obesity-induced transcriptional changes could alter the placental and the hepatic epigenome, leading to FGR. Preconceptional weight loss appears beneficial to fetal growth, but some effects of previous obesity were retained in offspring phenotype.Electronic supplementary materialThe online version of this article (doi:10.1186/s13148-016-0188-3) contains supplementary material, which is available to authorized users.

show abstract

“…Three studies did not report whether the tissue was collected uniformly from the medial or lateral segments of the placenta (Keleher et al, 2021;Mina et al, 2015;Räikkönen et al, 2014) although tissue inflammation has been shown to be more prone in the lateral sections (Burton et al, 2014). Likewise, three of the studies (Keleher et al, 2021;Mina et al, 2015;Muramatsu-Kato et al, 2014) did not report on the sampling time interval, increasing the risk that placental mRNA degradation could have interfered with the results (Burton et al, 2014;Freedman et al, 2021). Furthermore, in the Finish studies (Räikkönen et al, 2014), information on the pregnant women's nutritional habits was not reported, even though licorice, a common exposure in Finland (Räikkönen et al, 2009(Räikkönen et al, , 2010Strandberg et al, 2001), is a potent inhibitor of HSD11β2 and to some extent, an inhibitor of HSD11β1 (Chapman et al, 2013;Räikkönen et al, 2017).…”

Section: Limitationsmentioning

confidence: 99%

Obesity in pregnancy—Long‐term effects on offspring hypothalamic‐pituitary‐adrenal axis and associations with placental cortisol metabolism: A systematic review

Volqvartz,

Andersen,

Pedersen

et al. 2023

Eur J of Neuroscience

View full text Add to dashboard Cite

Obesity, affecting one in three pregnant women worldwide, is not only a major obstetric risk factor. The resulting low‐grade inflammation may have a long‐term impact on the offspring's HPA axis through dysregulation of maternal, placental and fetal corticosteroid metabolism, and children born of obese mothers have increased risk of diabetes and cardiovascular disease. The long‐term effects of maternal obesity on offspring neurodevelopment are, however, undetermined and could depend on the specific effects on placental and fetal cortisol metabolism. This systematic review evaluates how maternal obesity affects placental cortisol metabolism and the offspring's HPA axis. Pubmed, Embase and Scopus were searched for original studies on maternal BMI, obesity, and cortisol metabolism and transfer. Fifteen studies were included after the screening of 4556 identified records. Studies were small with heterogeneous exposures and outcomes. Two studies found that maternal obesity reduced placental HSD11β2 activity. In one study, umbilical cord blood cortisol levels were affected by maternal BMI. In three studies, an altered cortisol response was consistently seen among offspring in childhood (n = 2) or adulthood (n = 1). Maternal BMI was not associated with placental HSD11β1 or HSD11β2 mRNA expression, or placental HSD11β2 methylation. In conclusion, high maternal BMI is associated with reduced placental HSD11β2 activity and a dampened cortisol level among offspring, but the data is sparse. Further investigations are needed to clarify whether the HPA axis is affected by prenatal factors including maternal obesity and investigate if adverse effects can be ameliorated by optimising the intrauterine environment.

show abstract

Comparison between placental gene expression of 11β‐hydroxysteroid dehydrogenases and infantile growth at 10 months of age

Cited by 11 publications

References 32 publications

Neuroendocrinological and Epigenetic Mechanisms Subserving Autonomic Imbalance and HPA Dysfunction in the Metabolic Syndrome

Neuroendocrinological and Epigenetic Mechanisms Subserving Autonomic Imbalance and HPA Dysfunction in the Metabolic Syndrome

Expression of epigenetic machinery genes is sensitive to maternal obesity and weight loss in relation to fetal growth in mice

Obesity in pregnancy—Long‐term effects on offspring hypothalamic‐pituitary‐adrenal axis and associations with placental cortisol metabolism: A systematic review

Contact Info

Product

Resources

About