期刊
JOURNAL OF DEVELOPMENTAL ORIGINS OF HEALTH AND DISEASE
卷 13, 期 6, 页码 683-694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
- NHMRC
- University of Western Australia
- Curtin University
- Telethon Kids Institute
- Women and Infants Research Foundation
- Edith Cowan University
- Murdoch University
- University of Notre Dame Australia
- Raine Medical Research Foundation
- Canadian Institutes of Health Research -CIHR [MOP-82893]
- National Health and Medical Research Council of Australia [634445, 634509, 1021105]
- Canadian Institutes of Health Research [MOP82893]
- Ophthalmic Research Institute of Australia (ORIA)
- Alcon Research Institute
- Lions Eye Institute
- Australian Foundation for the Prevention of Blindness
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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