4.0 Article

Defining the role of the hypothalamic-pituitary-adrenal axis in the relationship between fetal growth and adult cardiometabolic outcomes

出版社

CAMBRIDGE UNIV PRESS
DOI: 10.1017/S2040174422000186

关键词

Hypothalamic-pituitary-adrenal axis; DoHAD; fetal growth; cardiometabolic; Trier Social Stress Test

资金

  1. NHMRC
  2. University of Western Australia
  3. Curtin University
  4. Telethon Kids Institute
  5. Women and Infants Research Foundation
  6. Edith Cowan University
  7. Murdoch University
  8. University of Notre Dame Australia
  9. Raine Medical Research Foundation
  10. Canadian Institutes of Health Research -CIHR [MOP-82893]
  11. National Health and Medical Research Council of Australia [634445, 634509, 1021105]
  12. Canadian Institutes of Health Research [MOP82893]
  13. Ophthalmic Research Institute of Australia (ORIA)
  14. Alcon Research Institute
  15. Lions Eye Institute
  16. Australian Foundation for the Prevention of Blindness

向作者/读者索取更多资源

Animal and human data show independent relationships between fetal growth, HPA-A function, and adult cardiometabolic outcomes. While the association between fetal growth and adult cardiometabolic outcomes is well-established, the specific role of HPA-A in these relationships remains unclear.
Animal and human data demonstrate independent relationships between fetal growth, hypothalamic-pituitary-adrenal axis function (HPA-A) and adult cardiometabolic outcomes. While the association between fetal growth and adult cardiometabolic outcomes is well-established, the role of the HPA-A in these relationships is unclear. This study aims to determine whether HPA-A function mediates or moderates this relationship. Approximately 2900 pregnant women were recruited between 1989-1991 in the Raine Study. Detailed anthropometric data was collected at birth (per cent optimal birthweight [POBW]). The Trier Social Stress Test was administered to the offspring (Generation 2; Gen2) at 18 years; HPA-A responses were determined (reactive responders [RR], anticipatory responders [AR] and non-responders [NR]). Cardiometabolic parameters (BMI, systolic BP [sBP] and LDL cholesterol) were measured at 20 years. Regression modelling demonstrated linear associations between POBW and BMI and sBP; quadratic associations were observed for LDL cholesterol. For every 10% increase in POBW, there was a 0.54 unit increase in BMI (standard error [SE] 0.15) and a 0.65 unit decrease in sBP (SE 0.34). The interaction between participant's fetal growth and HPA-A phenotype was strongest for sBP in young adulthood. Interactions for BMI and LDL-C were non-significant. Decomposition of the total effect revealed no causal evidence of mediation or moderation.

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