Parent-of-origin effects in the life-course evolution of cardiometabolic traits
Authors' conclusion
Our study provides proof of concept of the existence of parent-of-origin effects on cardiometabolic traits from birth, through childhood and puberty, until adult age. Our results indicate a predominantly maternal influence on intrauterine, pubertal and reproductive-age metabolism in the offspring. While the longitudinal analysis indicated a maternal bias for the macronutrients (glucose and lipids), and a paternal bias for glucose-insulin metabolism, the cross-sectional analysis revealed a transition between parental influence across physiological stages. This dynamic relationship may have its origins in the life-history theory of evolution, and could inform strategies for primordial prevention aimed at curbing the rising burden of cardiometabolic disease. Further studies are needed to determine the mechanisms underlying such effects.
Study context
- Population
- Offspring and parents of the Pune Maternal Nutrition Study birth cohort, studied from birth and followed up for 24 years
- Exposure
- Maternal vs paternal effects on offspring cardiometabolic traits
- Outcome
- Parent-of-origin effects on cardiometabolic traits
Methodological detailsserial measurements, cross-sectional and longitudinal analyses, replication cohort (Pune Children's Study)
- Serial measurements
- Cross-sectional and longitudinal analyses
- Replication cohort (Pune Children's Study)
Main finding
As reported in the abstract
- Birthweight showed a maternal parent-of-origin effect
- At 24 years, maternal bias for some obesity-related traits in daughters; paternal bias for WHR in sons
- Skinfold thickness in daughters shifted from paternal bias at 6 years to maternal bias at 24 years
- Fasting glucose and lipids showed maternal bias at 6, 12 and 24 years
- Fasting insulin and HOMA2-S: negative maternal effect at 6 years transitioned to a positive one at 12 years
- HOMA2-B: paternal effect at 6 years transitioned to maternal at 12 years, remaining so at 24 years
- Longitudinal modelling: stronger paternal effects over time for fasting insulin and HOMA indices, maternal effects for glucose and lipids
Observational data: associations, not effects.
Further findings
Replication in Pune Children's Study cohort
- Some of these findings were also observed in the Pune Children's Study cohort
Genetic parent-of-origin effects (KCNQ1 locus)
- KCNQ1 variants showed a maternal parent-of-origin effect on birthweight, HOMA2-B at 12 years, and lipids at 6 and 12 years
Original publication
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