Born from pre-eclamptic pregnancies predisposes infants to altered cortisol metabolism in the first postnatal year
Pre-eclampsia leads to disturbed fetal organ development, including metabolic syndrome, attributed to altered pituitary-adrenal feedback loop. We measured cortisol metabolites in infants born from pre-eclamptic and normotensive women and hypothesised that glucocorticoid exposure would be exaggerated...
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BioScientifica
2015
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| Online Access: | https://eprints.nottingham.ac.uk/44332/ |
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| author | Broughton Pipkin, Fiona Mistry, Hiten D. Roy, Chandrima Dick, Bernhard Waugh, Jason Chikhi, Rebecca Kurlak, L.O. Mohaupt, Markus |
| author_facet | Broughton Pipkin, Fiona Mistry, Hiten D. Roy, Chandrima Dick, Bernhard Waugh, Jason Chikhi, Rebecca Kurlak, L.O. Mohaupt, Markus |
| author_sort | Broughton Pipkin, Fiona |
| building | Nottingham Research Data Repository |
| collection | Online Access |
| description | Pre-eclampsia leads to disturbed fetal organ development, including metabolic syndrome, attributed to altered pituitary-adrenal feedback loop. We measured cortisol metabolites in infants born from pre-eclamptic and normotensive women and hypothesised that glucocorticoid exposure would be exaggerated in the former. Twenty-four hour urine was collected from infants at months 3 and 12. Cortisol metabolites and apparent enzyme activities were analysed by gas chromatography-mass spectrometry. From 3 to 12 months, excretion of THS, THF and pregnandiol had risen in both groups; THF also rose in the pre-eclamptic group. No difference was observed with respect to timing of the visit or to hypertensive status for THE or total F metabolites (P>0.05). All apparent enzymes activities, except 17α-hydroxylase, were lower in infants at 12 compared to 3 months in the normotensive group. In the pre-eclamptic group, only 11β-HSD activities were lower at 12 months.17α-hydroxylase and 11β-HSD activities of tetrahydro metabolites were higher in the pre-eclamptic group at 3 months (P<0.05). 11β-hydroxylase activity increased in the pre-eclamptic group at 12 months. Cortisol excretion, determined by increased 11β-hydroxylase, compensates for high 11β-HSD-dependent cortisol degradation at 3 months and at 12 months counterbalances the reduced cortisol substrate availability in infants born from pre-eclamptic mothers. |
| first_indexed | 2025-11-14T19:55:12Z |
| format | Article |
| id | nottingham-44332 |
| institution | University of Nottingham Malaysia Campus |
| institution_category | Local University |
| last_indexed | 2025-11-14T19:55:12Z |
| publishDate | 2015 |
| publisher | BioScientifica |
| recordtype | eprints |
| repository_type | Digital Repository |
| spelling | nottingham-443322024-08-15T15:17:47Z https://eprints.nottingham.ac.uk/44332/ Born from pre-eclamptic pregnancies predisposes infants to altered cortisol metabolism in the first postnatal year Broughton Pipkin, Fiona Mistry, Hiten D. Roy, Chandrima Dick, Bernhard Waugh, Jason Chikhi, Rebecca Kurlak, L.O. Mohaupt, Markus Pre-eclampsia leads to disturbed fetal organ development, including metabolic syndrome, attributed to altered pituitary-adrenal feedback loop. We measured cortisol metabolites in infants born from pre-eclamptic and normotensive women and hypothesised that glucocorticoid exposure would be exaggerated in the former. Twenty-four hour urine was collected from infants at months 3 and 12. Cortisol metabolites and apparent enzyme activities were analysed by gas chromatography-mass spectrometry. From 3 to 12 months, excretion of THS, THF and pregnandiol had risen in both groups; THF also rose in the pre-eclamptic group. No difference was observed with respect to timing of the visit or to hypertensive status for THE or total F metabolites (P>0.05). All apparent enzymes activities, except 17α-hydroxylase, were lower in infants at 12 compared to 3 months in the normotensive group. In the pre-eclamptic group, only 11β-HSD activities were lower at 12 months.17α-hydroxylase and 11β-HSD activities of tetrahydro metabolites were higher in the pre-eclamptic group at 3 months (P<0.05). 11β-hydroxylase activity increased in the pre-eclamptic group at 12 months. Cortisol excretion, determined by increased 11β-hydroxylase, compensates for high 11β-HSD-dependent cortisol degradation at 3 months and at 12 months counterbalances the reduced cortisol substrate availability in infants born from pre-eclamptic mothers. BioScientifica 2015-12-04 Article PeerReviewed Broughton Pipkin, Fiona, Mistry, Hiten D., Roy, Chandrima, Dick, Bernhard, Waugh, Jason, Chikhi, Rebecca, Kurlak, L.O. and Mohaupt, Markus (2015) Born from pre-eclamptic pregnancies predisposes infants to altered cortisol metabolism in the first postnatal year. Endcrine Connections, 4 (4). pp. 233-241. ISSN 2049-3614 steroid hormones; pre-eclampsia; infants; urine http://www.endocrineconnections.com/content/4/4/233.short doi:10.1530/EC-15-0084 doi:10.1530/EC-15-0084 |
| spellingShingle | steroid hormones; pre-eclampsia; infants; urine Broughton Pipkin, Fiona Mistry, Hiten D. Roy, Chandrima Dick, Bernhard Waugh, Jason Chikhi, Rebecca Kurlak, L.O. Mohaupt, Markus Born from pre-eclamptic pregnancies predisposes infants to altered cortisol metabolism in the first postnatal year |
| title | Born from pre-eclamptic pregnancies predisposes infants to altered cortisol metabolism in the first postnatal year |
| title_full | Born from pre-eclamptic pregnancies predisposes infants to altered cortisol metabolism in the first postnatal year |
| title_fullStr | Born from pre-eclamptic pregnancies predisposes infants to altered cortisol metabolism in the first postnatal year |
| title_full_unstemmed | Born from pre-eclamptic pregnancies predisposes infants to altered cortisol metabolism in the first postnatal year |
| title_short | Born from pre-eclamptic pregnancies predisposes infants to altered cortisol metabolism in the first postnatal year |
| title_sort | born from pre-eclamptic pregnancies predisposes infants to altered cortisol metabolism in the first postnatal year |
| topic | steroid hormones; pre-eclampsia; infants; urine |
| url | https://eprints.nottingham.ac.uk/44332/ https://eprints.nottingham.ac.uk/44332/ https://eprints.nottingham.ac.uk/44332/ |