High-fat diet and chronic stress aggravate adrenal function abnormality induced by prenatal caffeine exposure in male offspring rats

Zheng, He; Lv, Feng; Ding, Yong; Huang, Hegui; Liu, Lian; Zhu, Chunyan; Lei, Youyin; Zhang, Li; Si, Cai; Wang, Hui

doi:10.1038/s41598-017-14881-0

Cited by 27 publications

(11 citation statements)

References 52 publications

(58 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Similar to our current results, IUGR male rats exposed in utero to maternal tobacco smoke also have increased visceral adiposity in association with increased circulating corticosterone without changing GR-α protein levels 66 . Offspring HFD feeding alone did not change circulating corticosterone levels or 11-β HSD 1 or GR-α mRNA levels in adult rats 79 . In GR knock-out mice, obesity resulting from HFD feeding does not require the GR , whereas obesity resulting from exogenous glucocorticoid administration requires an intact GR , emphasizing the importance of multiple pathways to increased adiposity 80 .…”

Section: Discussionsupporting

confidence: 89%

“…66 Offspring HFD feeding alone did not change circulating corticosterone levels or 11-β HSD 1 or GR-α mRNA levels in adult rats. 79 In GR knock-out mice, obesity resulting from HFD feeding does not require the GR, whereas obesity resulting from exogenous glucocorticoid administration requires an intact GR, emphasizing the importance of multiple pathways to increased adiposity. 80 In our current study, a maternal HFD with or without a post-weaning HFD in non-IUGR male rats (NHR and NHH) increased visceral adiposity and adipocyte size, without changing circulating corticosterone or visceral adipose 11-β HSD 1 protein.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Intrauterine growth restriction combined with a maternal high-fat diet increased adiposity and serum corticosterone levels in adult rat offspring

Zinkhan

Callaway

et al. 2018

J Dev Orig Health Dis

View full text Add to dashboard Cite

Intrauterine growth restriction (IUGR) and fetal exposure to a maternal high-fat diet (HFD) independently increase the risk of developing obesity in adulthood. Excess glucocorticoids increase obesity. We hypothesized that surgically induced IUGR combined with an HFD would increase adiposity and glucocorticoids more than in non-IUGR offspring combined with the same HFD, findings that would persist despite weaning to a regular diet. Non-IUGR (N) and IUGR (I) rat offspring from dams fed either regular rat chow (R) or an HFD (H) were weaned to either a regular rat chow or an HFD. For non-IUGR and IUGR rats, this study design resulted in three diet groups: offspring from dams fed a regular diet and weaned to a regular diet (NRR and IRR), offspring rats from dams fed an HFD and weaned to a regular diet (NHR and IHR) and offspring from dams fed an HFD and weaned to an HFD (NHH and IHH). Magnetic resonance imaging or fasting visceral and subcutaneous adipose tissue collection occurred at postnatal day 60. IHH male rats had greater adiposity than NHH males, findings that were only partly normalized by weaning to a regular chow. IHH male rats had a 10-fold increase in serum corticosterone levels. IHH female rats had increased adiposity and serum triglycerides. We conclude that IUGR combined with an HFD throughout life increased adiposity, glucocorticoids and triglycerides in a sex-specific manner. Our data suggest that one mechanism through which the perinatal environment programs increased adiposity in IHH male rats may be via increased systemic glucocorticoids.

show abstract

Section: Discussionsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 99%

Intrauterine growth restriction combined with a maternal high-fat diet increased adiposity and serum corticosterone levels in adult rat offspring

Zinkhan

Callaway

et al. 2018

J Dev Orig Health Dis

View full text Add to dashboard Cite

show abstract

“…Moreover, liver TG and TC in the CON group were significantly higher than in the BLK group. Persistent exposure to glucocorticoids induces portal circulation of many fats and promotes ectopic fat storage in the liver and vascular tissues (Dallman et al, 2003;He et al, 2017). Our data showed that serum corticosterone (Fig.…”

Section: Discussionsupporting

confidence: 51%

Effects of <i>p</i>-Hydroxybenzaldehyde and <i>p</i>-Hydroxyacetophenone from Non-centrifuged Cane Sugar, Kokuto, on Serum Corticosterone, and Liver Conditions in Chronically Stressed Mice Fed with a High-fat Diet

Kinjo

Wada

et al. 2020

FSTR

View full text Add to dashboard Cite

In previous studies, the non-sugar component (NSC) fraction, analyzed as 50 % methanol extract from Kokuto, showed a high in vitro antioxidant activity and strong anti-stress effect in acutely stressed mice. In addition, p-hydroxybenzaldehyde (HBA) and p-hydroxyacetophenone (HAP) were determined to be some of the antioxidative compounds in the NSC fraction. Therefore, the aim of the present study was to investigate whether NSC fraction, HBA and HAP could suppress stress response and the changes of hepatic lipids in chronically stressed mice fed a high fat diet. The results of the present study show that the NSC fraction has a high antioxidant activity in vitro, and oral administration of the fraction and HAP suppressed the secretion of stress hormone in the chronically stressed mice. We also found that the two phenolic compounds prevented hepatic lipid accumulation and peroxidation in the stressed mice.

show abstract

“…Epidemiological investigations have proved that prenatal caffeine exposure (PCE) can cause toxic effects of reproduction and fetal development, such as the increased risk of congenital malformations, premature delivery, spontaneous abortion, IUGR, and susceptibility to chronic diseases [ 21 , 22 ]. Our animal experiments also demonstrated that PCE could not only increase maternal glucocorticoid levels but also cause fetal overexposure to glucocorticoid by inhibiting placental 11β-HSD2, leading to the occurrence of IUGR and susceptibility to multiple chronic diseases in adult offspring [ 16 , 23 – 26 ]. However, whether caffeine causes IUGR by affecting placental P-gp has not been reported yet.…”

Section: Introductionmentioning

confidence: 83%

P-gp expression inhibition mediates placental glucocorticoid barrier opening and fetal weight loss

Fang

et al. 2021

BMC Med

Self Cite

View full text Add to dashboard Cite

Background Prenatal adverse environments can cause fetal intrauterine growth retardation (IUGR) and higher susceptibility to multiple diseases after birth, related to multi-organ development programming changes mediated by intrauterine overexposure to maternal glucocorticoids. As a glucocorticoid barrier, P-glycoprotein (P-gp) is highly expressed in placental syncytiotrophoblasts; however, the effect of P-gp on the occurrence of IUGR remains unclear. Methods Human placenta and fetal cord blood samples of IUGR fetuses were collected, and the related indexes were detected. Pregnant Wistar rats were administered with 30 mg/kg·d (low dose) and 120 mg/kg·d (high dose) caffeine from gestational day (GD) 9 to 20 to construct the rat IUGR model. Pregnant mice were administered with caffeine (120 mg/kg·d) separately or combined with sodium ferulate (50 mg/kg·d) from gestational day GD 9 to 18 to confirm the intervention target on fetal weight loss caused by prenatal caffeine exposure (PCE). The fetal serum/placental corticosterone level, placental P-gp expression, and related indicator changes were analyzed. In vitro, primary human trophoblasts and BeWo cells were used to confirm the effect of caffeine on P-gp and its mechanism. Results The placental P-gp expression was significantly reduced, but the umbilical cord blood cortisol level was increased in clinical samples of the IUGR neonates, which were positively and negatively correlated with the neonatal birth weight, respectively. Meanwhile, in the PCE-induced IUGR rat model, the placental P-gp expression of IUGR rats was decreased while the corticosterone levels of the placentas/fetal blood were increased, which were positively and negatively correlated with the decreased placental/fetal weights, respectively. Combined with the PCE-induced IUGR rat model, in vitro caffeine-treated placental trophoblasts, we confirmed that caffeine decreased the histone acetylation and expression of P-gp via RYR/JNK/YB-1/P300 pathway, which inhibited placental and fetal development. We further demonstrated that P-gp inducer sodium ferulate could reverse the inhibitory effect of caffeine on the fetal body/placental weight. Finally, clinical specimens and other animal models of IUGR also confirmed that the JNK/YB-1 pathway is a co-regulatory mechanism of P-gp expression inhibition, among which the expression of YB-1 is the most stable. Therefore, we proposed that YB-1 could be used as the potential early warning target for the opening of the placental glucocorticoid barrier, the occurrence of IUGR, and the susceptibility of a variety of diseases. Conclusions This study, for the first time, clarified the critical role and epigenetic regulation mechanism of P-gp in mediating the opening mechanism of the placental glucocorticoid barrier, providing a novel idea for exploring the early warning, prevention, and treatment strategies of IUGR.

show abstract

High-fat diet and chronic stress aggravate adrenal function abnormality induced by prenatal caffeine exposure in male offspring rats

Cited by 27 publications

References 52 publications

Intrauterine growth restriction combined with a maternal high-fat diet increased adiposity and serum corticosterone levels in adult rat offspring

Intrauterine growth restriction combined with a maternal high-fat diet increased adiposity and serum corticosterone levels in adult rat offspring

Effects of <i>p</i>-Hydroxybenzaldehyde and <i>p</i>-Hydroxyacetophenone from Non-centrifuged Cane Sugar, Kokuto, on Serum Corticosterone, and Liver Conditions in Chronically Stressed Mice Fed with a High-fat Diet

P-gp expression inhibition mediates placental glucocorticoid barrier opening and fetal weight loss

Contact Info

Product

Resources

About