P Acosta-Manzano1,2, B Leopold-Posch3, D Simmons4, R Devlieger5, S Galjaard5,6, R Corcoy7, J M Adelantado8, F Dunne9, J Harreiter10, A Kautzky-Willer10, P Damm11, E R Mathiesen11, D M Jensen12,13,14, L L Andersen13,14, M Tanvig13,14, A Lapolla15, M G Dalfra15, A Bertolotto16, E Wender-Ozegowska17, A Zawiejska18, D J Hill19, F J Snoek20, Jgm Jelsma21, G Desoye3, Mnm van Poppel22. 1. PA-HELP 'Physical Activity for Health Promotion, CTS-1018' Research Group, Sport and Health University Research Institute (iMUDS), University of Granada, Granada, Spain. 2. Department of Physical Education and Sports, Faculty of Sports Science, University of Granada, Granada, Spain. 3. Department of Obstetrics and Gynaecology, Medical University Graz, Graz, Austria. 4. Western Sydney University, Campbelltown, New South Wales, Australia. 5. Department of Development and Regeneration: Pregnancy, Fetus and Neonate, Gynaecology and Obstetrics, KU Leuven, University Hospitals Leuven, Leuven, Belgium. 6. Department of Obstetrics and Gynaecology, Division of Obstetrics and Prenatal Medicine, Erasmus MC, University Medical Centre Rotterdam, Rotterdam, the Netherlands. 7. CIBER Bioengineering, Biomaterials and Nanomedicine, Instituto de Salud Carlos III, Zaragoza, Spain. 8. Institut de Recerca de l'Hospital de la Santa Creu i Sant Pau, Barcelona, Spain. 9. Galway Diabetes Research Centre (GDRC) and National University of Ireland, Galway, Ireland. 10. Gender Medicine Unit, Endocrinology and Metabolism, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria. 11. Departments of Endocrinology and Obstetrics, Rigshospitalet and Department of Clinical Medicine, Centre for Pregnant Women with Diabetes, University of Copenhagen, Copenhagen, Denmark. 12. Steno Diabetes Centre Odense, Odense University Hospital, Odense, Denmark. 13. Department of Gynaecology and Obstetrics, Odense University Hospital, Odense, Denmark. 14. Department of Clinical Research, Faculty of Health Science, University of Southern Denmark, Odense, Denmark. 15. Department of Medical and Surgical Sciences, Università degli Studi di Padova, Padua, Italy. 16. Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy. 17. Department of Reproduction, Poznan University of Medical Sciences, Poznan, Poland. 18. Chair of Medical Education, Department of Medical Simulation, Poznan University of Medical Sciences, Poznan, Poland. 19. Lawson Health Research Institute, London, Ontario, Canada. 20. Department of Medical Psychology, Amsterdam Public Health Research Institute, Amsterdam University Medical Centres, VU University, Amsterdam, the Netherlands. 21. Amsterdam UMC, Vrije Universiteit Amsterdam, Department of Public and Occupational Health, Amsterdam Public Health Research Institute, Amsterdam, the Netherlands. 22. Institute of Human Movement Science, Sport and Health, University of Graz, Graz, Austria.
Abstract
OBJECTIVE: We aimed to explore: (i) the association of sedentary time (ST) and physical activity (PA) during pregnancy with the placental expression of genes related to glucose and lipid metabolism in pregnant women who are obese; (ii) maternal metabolic factors mediating changes in these placental transcripts; and (iii) cord blood markers related to the mRNAs mediating neonatal adiposity. DESIGN: Multicentre randomised controlled trial. SETTING: Hospitals in nine European countries. POPULATION: A cohort of 112 pregnant women with placental tissue. METHODS: Both ST and moderate-to-vigorous PA (MVPA) levels were measured objectively using accelerometry at three time periods during pregnancy. MAIN OUTCOME MEASURES: Placental mRNAs (FATP2, FATP3, FABP4, GLUT1 and PPAR-γ) were measured with NanoString technology. Maternal and fetal metabolic markers and neonatal adiposity were assessed. RESULTS: Longer periods of ST, especially in early to middle pregnancy, was associated with lower placental FATP2 and FATP3 expression (P < 0.05), whereas MVPA at baseline was inversely associated with GLUT1 mRNA (P = 0.02). Although placental FATP2 and FATP3 expression were regulated by the insulin-glucose axis (P < 0.05), no maternal metabolic marker mediated the association of ST/MVPA with placental mRNAs (P > 0.05). Additionally, placental FATP2 expression was inversely associated with cord blood triglycerides and free fatty acids (FFAs; P < 0.01). No cord blood marker mediated neonatal adiposity except for cord blood leptin, which mediated the effects of PPAR-γ on neonatal sum of skinfolds (P < 0.05). CONCLUSIONS: In early to middle pregnancy, ST is associated with the expression of placental genes linked to lipid transport. PA is hardly related to transporter mRNAs. Strategies aimed at reducing sedentary behaviour during pregnancy could modulate placental gene expression, which may help to prevent unfavourable fetal and maternal pregnancy outcomes. TWEETABLE ABSTRACT: Reducing sedentary behaviour in pregnancy might modulate placental expression of genes related to lipid metabolism in women who are obese.
OBJECTIVE: We aimed to explore: (i) the association of sedentary time (ST) and physical activity (PA) during pregnancy with the placental expression of genes related to glucose and lipid metabolism in pregnant women who are obese; (ii) maternal metabolic factors mediating changes in these placental transcripts; and (iii) cord blood markers related to the mRNAs mediating neonatal adiposity. DESIGN: Multicentre randomised controlled trial. SETTING: Hospitals in nine European countries. POPULATION: A cohort of 112 pregnant women with placental tissue. METHODS: Both ST and moderate-to-vigorous PA (MVPA) levels were measured objectively using accelerometry at three time periods during pregnancy. MAIN OUTCOME MEASURES: Placental mRNAs (FATP2, FATP3, FABP4, GLUT1 and PPAR-γ) were measured with NanoString technology. Maternal and fetal metabolic markers and neonatal adiposity were assessed. RESULTS: Longer periods of ST, especially in early to middle pregnancy, was associated with lower placental FATP2 and FATP3 expression (P < 0.05), whereas MVPA at baseline was inversely associated with GLUT1 mRNA (P = 0.02). Although placental FATP2 and FATP3 expression were regulated by the insulin-glucose axis (P < 0.05), no maternal metabolic marker mediated the association of ST/MVPA with placental mRNAs (P > 0.05). Additionally, placental FATP2 expression was inversely associated with cord blood triglycerides and free fatty acids (FFAs; P < 0.01). No cord blood marker mediated neonatal adiposity except for cord blood leptin, which mediated the effects of PPAR-γ on neonatal sum of skinfolds (P < 0.05). CONCLUSIONS: In early to middle pregnancy, ST is associated with the expression of placental genes linked to lipid transport. PA is hardly related to transporter mRNAs. Strategies aimed at reducing sedentary behaviour during pregnancy could modulate placental gene expression, which may help to prevent unfavourable fetal and maternal pregnancy outcomes. TWEETABLE ABSTRACT: Reducing sedentary behaviour in pregnancy might modulate placental expression of genes related to lipid metabolism in women who are obese.
Authors: Saghi Zafaranieh; Anna M Dieberger; Barbara Leopold-Posch; Berthold Huppertz; Sebastian Granitzer; Markus Hengstschläger; Claudia Gundacker; Gernot Desoye; Mireille N M van Poppel Journal: Biomedicines Date: 2022-05-05
Authors: Cody J Strom; Samantha M McDonald; Mary-Margaret Remchak; Kimberly A Kew; Blake R Rushing; Joseph A Houmard; David A Tulis; Roman Pawlak; George A Kelley; Lisa Chasan-Taber; Edward Newton; Christy Isler; James DeVente; Madigan Raper; Linda E May Journal: Int J Environ Res Public Health Date: 2022-07-07 Impact factor: 4.614