The effects of an obesogenic diet during pregnancy on fetal growth and placental gene expression are gestation dependent

King, Vicky; Hibbert, Nanette; Norman, Jane E.; Drake, Amanda J.

doi:10.1016/j.placenta.2013.09.006

Cited by 34 publications

(29 citation statements)

References 25 publications

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“…Whether there is a genetic susceptibility to decreased ABCB1 activity in this cohort of SO women is unknown. Notably, the observations of increased placental igf2, nr3c1 and igf2r in rodent models receiving either an obesogenic diet during pregnancy (Sferruzzi-Perri et al, 2013) or a chronic obesogenic diet (King et al, 2013) were restricted to mid-gestation with no differences at term. If there are similar transient changes in mRNA levels in mid gestation in human placenta, this may explain the lack of differences between lean and SO in our study using samples collected at term.…”

Section: Discussionmentioning

confidence: 99%

Maternal distress associates with placental genes regulating fetal glucocorticoid exposure and IGF2: Role of obesity and sex

Mina

Räikkönen

Riley

et al. 2015

Psychoneuroendocrinology

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Maternal emotional distress symptoms, including life satisfaction, anxiety and depressed mood, are worse in Severely Obese (SO) than lean pregnancy and may alter placental genes regulating fetal glucocorticoid exposure and placental growth. We hypothesised that the associations between increased maternal distress symptoms and changes in placental gene expression including IGF2 and genes regulating fetal glucocorticoid exposure are more pronounced in SO pregnancy. We also considered whether there were sex-specific effects. Placental mRNA levels of 11β-HSDs, NR3C1-α, NR3C2, ABC transporters, mTOR and the IGF2 family were measured in term placental samples from 43 lean (BMI≤25kg/m(2)) and 50 SO (BMI≥40kg/m(2)) women, in whom distress symptoms were prospectively evaluated during pregnancy. The mRNA levels of genes with a similar role in regulating fetal glucocorticoid exposure were strongly inter-correlated. Increased maternal distress symptoms associated with increased NR3C2 and IGF2 isoform 1(IGF2-1) in both lean and SO group (p≤0.05). Increased distress was associated with higher ABCB1 and ABCG2 mRNA levels in SO but lower ABCB1 and higher 11β-HSD1 mRNA levels in lean (p≤0.05) suggesting a protective adaptive response in SO placentas. Increased maternal distress associated with reduced mRNA levels of ABCB1, ABCG2, 11β-HSD2, NR3C1-α and IGF2-1 in placentas of female but not male offspring. The observed sex differences in placental responses suggest greater vulnerability of female fetuses to maternal distress with potentially greater fetal glucocorticoid exposure and excess IGF2. Further studies are needed to replicate these findings and to test whether this translates to potentially greater negative outcomes of maternal distress in female offspring in early childhood.

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Section: Discussionmentioning

confidence: 99%

Maternal distress associates with placental genes regulating fetal glucocorticoid exposure and IGF2: Role of obesity and sex

Mina

Räikkönen

Riley

et al. 2015

Psychoneuroendocrinology

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“…A previous study of the same strain of mice fed a diet with a higher fat content found reduced 11β-HSD2 activity in association with elevated maternal corticosterone [21], in contrast to the reduced maternal levels that we observed. Other studies of the same strain of mice have found that a higher fat diet either reduces 11β-HSD2 mRNA expression [22] or has no effect [26]. A maternal low-protein diet did not affect placental 11β-HSD2 expression or activity in mice [41], in contrast to other species.…”

Section: Discussionmentioning

confidence: 99%

“…We speculate that the mothers’ altered caloric intake was adequate to protect the fetuses from overgrowth and/ or that our dietary manipulation was not sufficiently severe to warrant changes in gene expression. However, the effects of maternal diet on nutrient transporter expression have been found to vary through gestation [22,23,26] and thus we cannot rule out the possibility that nutrient transport was altered earlier in pregnancy.…”

Section: Discussionmentioning

confidence: 99%

“…A reference sample was prepared by combining samples and was included in every assay to account for variation between assays. In addition to the mRNA levels of Hsd11b1 and Hsd11b2 , we also measured Slc38a2 , Slc27a4 , Slc2a1 , genes encoding neutral amino acid, long-chain fatty acid and glucose transporters, respectively, expressed in the placenta [23,26,35] and β-actin as a housekeeping gene. Primer sequences are shown in Table 1.…”

Section: Methodsmentioning

confidence: 99%

“…We also assessed the effects of the diet manipulation on pregnancy and other aspects of offspring programming frequently measured in other studies. In particular, we measured placental phosphorylation of protein kinase B (Akt) as a measure of insulin signaling [23–25] and placental expression of nutrient transporters [23,26], as well as metabolic traits of the offspring including food intake, energy expenditure and glucose tolerance [8]. Because leptin can affect 11β-HSD2 activity [27] and because glucocorticoids may regulate leptin expression [28], we also measured leptin in the maternal and fetal circulations.…”

Section: Introductionmentioning

confidence: 99%

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A maternal high-fat, high-sucrose diet has sex-specific effects on fetal glucocorticoids with little consequence for offspring metabolism and voluntary locomotor activity in mice

et al. 2017

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Maternal overnutrition and obesity during pregnancy can have long-term effects on offspring physiology and behaviour. These developmental programming effects may be mediated by fetal exposure to glucocorticoids, which is regulated in part by placental 11β-hydroxysteroid dehydrogenase (11β-HSD) type 1 and 2. We tested whether a maternal high-fat, high-sucrose diet would alter expression of placental 11β-HSD1 and 2, thereby increasing fetal exposure to maternal glucocorticoids, with downstream effects on offspring physiology and behaviour. C57BL/6J mice were fed a high-fat, high-sucrose (HFHS) diet or a nutrient-matched low-fat, no-sucrose control diet prior to and during pregnancy and lactation. At day 17 of gestation, HFHS dams had ~20% lower circulating corticosterone levels than controls. Furthermore, there was a significant interaction between maternal diet and fetal sex for circulating corticosterone levels in the fetuses, whereby HFHS males tended to have higher corticosterone than control males, with no effect in female fetuses. However, placental 11β-HSD1 or 11β-HSD2 expression did not differ between diets or show an interaction between diet and sex. To assess potential long-term consequences of this sex-specific effect on fetal corticosterone, we studied locomotor activity and metabolic traits in adult offspring. Despite a sex-specific effect of maternal diet on fetal glucocorticoids, there was little evidence of sex-specific effects on offspring physiology or behaviour, although HFHS offspring of both sexes had higher circulating corticosterone at 9 weeks of age. Our results suggest the existence of as yet unknown mechanisms that mitigate the effects of altered glucocorticoid exposure early in development, making offspring resilient to the potentially negative effects of a HFHS maternal diet.

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Prenatal Adversity Modulates the Quality of Maternal Care Via the Exposed Offspring

Roshan

2019

BioEssays

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Adversities in pregnancy, including poor diet and stress, are associated with increased risk of developing both metabolic and mental health disorders later in life, a phenomenon described as fetal programming or developmental origins of disease. Predominant hypotheses proposed to explain this relationship suggest that the adversity imposes direct changes to the developing fetus which are maintained after birth resulting in an increased susceptibility to ill health. However, during pregnancy the mother, the developing fetus, and the placenta are all exposed to the adversity. The same adversities linked to altered offspring outcome can also result in suboptimal maternal care, which is considered an independent adverse exposure for the offspring. Recent key experiments in mice reveal the potential of prenatal adversity to drive alterations in maternal care through abnormal maternal–pup interactions and via alterations in placental signaling. Together, these data highlight the critical importance of viewing fetal programming holistically paying attention to the intimate, bidirectional, and reiterative relationship between mothers and their offspring.

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The effects of an obesogenic diet during pregnancy on fetal growth and placental gene expression are gestation dependent

Cited by 34 publications

References 25 publications

Maternal distress associates with placental genes regulating fetal glucocorticoid exposure and IGF2: Role of obesity and sex

Maternal distress associates with placental genes regulating fetal glucocorticoid exposure and IGF2: Role of obesity and sex

A maternal high-fat, high-sucrose diet has sex-specific effects on fetal glucocorticoids with little consequence for offspring metabolism and voluntary locomotor activity in mice

Prenatal Adversity Modulates the Quality of Maternal Care Via the Exposed Offspring

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