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Placental 11β-HSD2 and Cardiometabolic Health Indicators in Infancy

Lu Chen1,2,3, Julie Guilmette2,4, Zhong-Cheng Luo5,2

  • 1Department of Obstetrics and Gynecology, Lunenfeld-Tanenbaum Research Institute, Prosserman Center for Population Health Research, Mount Sinai Hospital, and Institute of Health Policy, Management and Evaluation, University of Toronto, Toronto, Canada.

Diabetes Care
|March 6, 2019
PubMed

Insights

Higher placental 11β-hydroxysteroid dehydrogenase 2 (11β-HSD2) expression is linked to reduced infant insulin resistance (IR). This finding suggests a protective role for placental 11β-HSD2 in programming cardiometabolic health.

Area of Science:

  • Endocrinology
  • Perinatal Medicine
  • Metabolic Health

Background:

  • Fetal exposure to glucocorticoids may increase cardiometabolic risk.
  • Placental 11β-hydroxysteroid dehydrogenase 2 (11β-HSD2) acts as a barrier against excessive fetal glucocorticoid exposure.
  • The association between placental 11β-HSD2 levels and postnatal cardiometabolic health is unexplored.

Purpose of the Study:

  • To investigate the relationship between placental 11β-HSD2 expression and cardiometabolic health markers in infants at one year of age.
  • To determine if placental 11β-HSD2 levels are associated with insulin resistance (IR) and blood pressure (BP) in infancy.

Main Methods:

  • Prospective birth cohort study of 246 mother-infant pairs.
  • Measurement of placental 11β-HSD2 expression and maternal/cord plasma cortisol concentrations.
  • Assessment of infant outcomes at age 1 year, including HOMA of IR, BP, fasting insulin, HOMA β-cell function, carotid intima-media thickness, and anthropometric measures.

Main Results:

  • Placental 11β-HSD2 expression showed a negative correlation with infant HOMA-IR and fasting insulin.
  • A marginal negative correlation was observed between placental 11β-HSD2 expression and systolic BP.
  • Maternal cortisol correlated positively with carotid intima-media thickness, while cord cortisol correlated negatively with skinfold thickness.

Conclusions:

  • This study provides the first evidence linking higher placental 11β-HSD2 expression to lower infant insulin resistance.
  • The findings suggest a potential protective role of placental 11β-HSD2 in mitigating programming of cardiometabolic risk.
  • Further independent cohort studies are necessary to validate these novel findings.
Abstract

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