Psychoneuroendocrinology · 2026
Mediating role of maternal cortisol in the association between maternal serum creatinine and fetal cortisol exposure.
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Lin Ziyan, Zhang Zhiqi, Yang Guoping, Wang Nan, Peng Jinfu
Аннотация
BACKGROUND: Cortisol is the principal glucocorticoid regulated by the hypothalamic-pituitary-adrenal (HPA) axis and plays a crucial role in maintaining pregnancy and promoting fetal growth and development. Renal function is a key determinant of cortisol exposure. Given that serum creatinine serves as a key biomarker of renal function, it is plausible that maternal creatinine levels contribute to the regulation of fetal cortisol exposure, although the underlying mechanisms remain to be fully elucidated.
OBJECTIVE: This study was designed to (1) examine the association between maternal serum creatinine and umbilical cord blood cortisol levels, (2) assess the potential mediating role of maternal cortisol in this relationship, and (3) investigate corresponding changes in the protein expression of placental 11β-HSD1 and 11β-HSD2.
METHODS: This study employed a paired maternal-fetal design. At delivery, maternal serum, umbilical cord blood, and placental tissue were collected simultaneously from 103 mother-newborn pairs. Cortisol and cortisone levels in maternal and cord blood were measured, and protein expression of 11β-HSD1 and 11β-HSD2 in placental tissue was analyzed. Correlation and mediation analyses were performed to assess the relationships among maternal serum creatinine, maternal cortisol, and cord blood cortisol.
RESULTS: Each unit increase in maternal serum creatinine was associated with a significant decrease in cord blood cortisol levels. Maternal cortisol levels were positively correlated with cord blood cortisol. Mediation analysis showed that maternal cortisol mediated 31.75 % of the association between maternal creatinine and cord blood cortisol. In the high-creatinine conditions, placental expression of 11β-HSD1 was significantly decreased, while expression of 11β-HSD2 was increased.
CONCLUSION: Maternal cortisol showed evidence of partial mediation in the association between maternal renal function and fetal cortisol exposure. This observational finding highlights a potential link between maternal renal function and fetal glucocorticoid exposure and provides a basis for future studies to investigate the role of placental glucocorticoid regulation and fetal HPA axis development.
OBJECTIVE: This study was designed to (1) examine the association between maternal serum creatinine and umbilical cord blood cortisol levels, (2) assess the potential mediating role of maternal cortisol in this relationship, and (3) investigate corresponding changes in the protein expression of placental 11β-HSD1 and 11β-HSD2.
METHODS: This study employed a paired maternal-fetal design. At delivery, maternal serum, umbilical cord blood, and placental tissue were collected simultaneously from 103 mother-newborn pairs. Cortisol and cortisone levels in maternal and cord blood were measured, and protein expression of 11β-HSD1 and 11β-HSD2 in placental tissue was analyzed. Correlation and mediation analyses were performed to assess the relationships among maternal serum creatinine, maternal cortisol, and cord blood cortisol.
RESULTS: Each unit increase in maternal serum creatinine was associated with a significant decrease in cord blood cortisol levels. Maternal cortisol levels were positively correlated with cord blood cortisol. Mediation analysis showed that maternal cortisol mediated 31.75 % of the association between maternal creatinine and cord blood cortisol. In the high-creatinine conditions, placental expression of 11β-HSD1 was significantly decreased, while expression of 11β-HSD2 was increased.
CONCLUSION: Maternal cortisol showed evidence of partial mediation in the association between maternal renal function and fetal cortisol exposure. This observational finding highlights a potential link between maternal renal function and fetal glucocorticoid exposure and provides a basis for future studies to investigate the role of placental glucocorticoid regulation and fetal HPA axis development.