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Fetal exposure to high levels of corticosterone in a low birth weight rat model
Author(s) -
Hennington Bettye Sue,
Williamson Danielle T.,
Porter Nicholas K.,
Ojeda Norma B.,
Intapad Suttira,
McMillan Tiarra,
Arguello Irene,
Brown Andrew,
Wilkening Stephen,
Alexander Barbara T.
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.lb890
Subject(s) - corticosterone , fetus , endocrinology , medicine , placenta , western blot , birth weight , biology , andrology , pregnancy , hormone , biochemistry , gene , genetics
Fetal exposure to maternal steroids is suggested as a potential mechanism contributing to the developmental programming of adult CVD risk. 14‐day timed pregnant SD Dams were used for the RUPP while matched control SD females were subjected to sham surgeries. Corticosterone levels in Dam plasma were significantly higher in RUPP compared to E19 Control Dams. At P14, the corticosterone levels remained significantly higher in the RUPP compared to the Control Dams. Pups were sacrificed at E19, E20, and P14. E19 and E20 fetuses showed significant decrease in weight compared to the control fetuses. P14 IUGR showed significantly decreased weight compared to control pups. E19 and E20 placental weights significantly decreased in the RUPP compared to the control group. E19 and E20 placental efficiency significantly increased in the RUPP compared to control fetuses. No significant difference in plasma corticosterone between the E19, E20, and P14 IUGR compared to the Control groups. qPCR showed increased 11betaHSD2 message at E20 compared to Control placentas. Western blot analysis with kidney homogenates indicated significantly increased 11betaHSD2 in the P14 RUPP compared to Control Dams. The preliminary data suggests that while there is significant increase in plasma corticosterone in the RUPP compared to the Control Dams, the corticosterone is not crossing the placenta. The indication is that 11betaHSD2 may be part of the fetal protective mechanism; however, not the major mechanism.