Rodrigo A Lima1, Gernot Desoye2, David Simmons3,4, Roland Devlieger5, Sander Galjaard5,6, Rosa Corcoy7,8, Juan M Adelantado7,8, Fidelma Dunne9, Jürgen Harreiter10, Alexandra Kautzky-Willer10, Peter Damm11, Elisabeth R Mathiesen11, Dorte M Jensen12,13, Lise-Lotte T Andersen12,14, Mette Tanvig12,14, Annunziata Lapolla15, Maria G Dalfra15, Alessandra Bertolotto16, Urszula Manta17, Ewa Wender-Ozegowska17, Agnieszka Zawiejska17, David J Hill18, Frank J Snoek19, Judith G M Jelsma20, Mireille van Poppel1. 1. Institution of Sport Science, University of Graz, Graz, Austria. 2. Department of Obstetrics and Gynecology, Medizinische Universitaet Graz, Graz, Austria. 3. Western Sydney University, Campbelltown, New South Wales, Australia. 4. The Institute of Metabolic Science, Addenbrooke's Hospital, Cambridge, UK. 5. KU Leuven Department of Development and Regeneration: Pregnancy, Fetus and Neonate, Gynaecology and Obstetrics, University Hospitals Leuven, Leuven, Belgium. 6. Division of Obstetrics and Prenatal Medicine, Department of Obstetrics and Gynaecology, Erasmus MC, University Medical Centre Rotterdam, Rotterdam, The Netherlands. 7. Institut de Recerca de l´Hospital de la Santa Creu i Sant Pau, Barcelona, Spain. 8. CIBER Bioengineering, Biomaterials and Nanotechnology, Instituto de Salud Carlos III, Zaragoza, Spain. 9. Galway Diabetes Research Centre and College of Medicine Nursing and Health Sciences, 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, Faculty of Health and Medical Sciences, Center for Pregnant Women with Diabetes, Rigshospitalet, Institute of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark. 12. Department of Gynecology and Obstetrics, Odense University Hospital, University of Southern Denmark, Odense, Denmark. 13. Department of Clinical Research, Faculty of Health Sciences, Steno Diabetes Center Odense, Odense University Hospital, University of Southern Denmark, Odense, Denmark. 14. Department of Clinical Research, Faculty of Health Sciences, University of Southern Denmark, Odense, Denmark. 15. Universita Degli Studi di Padova, Padua, Italy. 16. Azienda Ospedaliero Universitaria - Pisa, Pisa, Italy. 17. Department of Reproduction, Poznan University of Medical Sciences, Poznan, Poland. 18. Recherche en Santé Lawson SA, Bronschhofen, Switzerland. 19. Department of Medical Psychology, Amsterdam Public Health research institute, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. 20. Department of Public and Occupational Health, Amsterdam Public Health Research Institute, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands.
Abstract
BACKGROUND: Although previous studies evaluated the association of maternal health parameters with neonatal adiposity, little is known regarding the complexity of the relationships among different maternal health parameters throughout pregnancy and its impact on neonatal adiposity. OBJECTIVES: To evaluate the direct and indirect associations between maternal insulin resistance during pregnancy, in women with obesity, and neonatal adiposity. In addition, associations between maternal fasting glucose, triglycerides (TG), non-esterified fatty acids (NEFA), and neonatal adiposity were also assessed. METHODS: This is a longitudinal, secondary analysis of the DALI study, an international project conducted in nine European countries with pregnant women with obesity. Maternal insulin resistance (HOMA-IR), fasting glucose, TG, and NEFA were measured three times during pregnancy (<20, 24-28, and 35-37 weeks of gestation). Offspring neonatal adiposity was estimated by the sum of four skinfolds. Structural equation modelling was conducted to evaluate the direct and indirect relationships among the variables of interest. RESULTS: Data on 657 mother-infant pairs (50.7% boys) were analysed. Neonatal boys exhibited lower mean sum of skinfolds compared to girls (20.3 mm, 95% CI 19.7, 21.0 vs 21.5 mm, 95% CI 20.8, 22.2). In boys, maternal HOMA-IR at <20 weeks was directly associated with neonatal adiposity (β = 0.35 mm, 95% CI 0.01, 0.70). In girls, maternal HOMA-IR at 24-28 weeks was only indirectly associated with neonatal adiposity, which implies that this association was mediated via maternal HOMA-IR, glucose, triglycerides, and NEFA during pregnancy (β = 0.26 mm, 95% CI 0.08, 0.44). CONCLUSIONS: The timing of the role of maternal insulin resistance on neonatal adiposity depends on fetal sex. Although the association was time-dependent, maternal insulin resistance was associated with neonatal adiposity in both sexes.
BACKGROUND: Although previous studies evaluated the association of maternal health parameters with neonatal adiposity, little is known regarding the complexity of the relationships among different maternal health parameters throughout pregnancy and its impact on neonatal adiposity. OBJECTIVES: To evaluate the direct and indirect associations between maternal insulin resistance during pregnancy, in women with obesity, and neonatal adiposity. In addition, associations between maternal fasting glucose, triglycerides (TG), non-esterified fatty acids (NEFA), and neonatal adiposity were also assessed. METHODS: This is a longitudinal, secondary analysis of the DALI study, an international project conducted in nine European countries with pregnant women with obesity. Maternal insulin resistance (HOMA-IR), fasting glucose, TG, and NEFA were measured three times during pregnancy (<20, 24-28, and 35-37 weeks of gestation). Offspring neonatal adiposity was estimated by the sum of four skinfolds. Structural equation modelling was conducted to evaluate the direct and indirect relationships among the variables of interest. RESULTS: Data on 657 mother-infant pairs (50.7% boys) were analysed. Neonatal boys exhibited lower mean sum of skinfolds compared to girls (20.3 mm, 95% CI 19.7, 21.0 vs 21.5 mm, 95% CI 20.8, 22.2). In boys, maternal HOMA-IR at <20 weeks was directly associated with neonatal adiposity (β = 0.35 mm, 95% CI 0.01, 0.70). In girls, maternal HOMA-IR at 24-28 weeks was only indirectly associated with neonatal adiposity, which implies that this association was mediated via maternal HOMA-IR, glucose, triglycerides, and NEFA during pregnancy (β = 0.26 mm, 95% CI 0.08, 0.44). CONCLUSIONS: The timing of the role of maternal insulin resistance on neonatal adiposity depends on fetal sex. Although the association was time-dependent, maternal insulin resistance was associated with neonatal adiposity in both sexes.
Authors: U M Schaefer-Graf; K Meitzner; H Ortega-Senovilla; K Graf; K Vetter; M Abou-Dakn; E Herrera Journal: Diabet Med Date: 2011-09 Impact factor: 4.359
Authors: Tessa L Crume; Allison L Shapiro; John T Brinton; Deborah H Glueck; Mercedes Martinez; Mary Kohn; Curtis Harrod; Jacob E Friedman; Dana Dabelea Journal: J Clin Endocrinol Metab Date: 2015-01-09 Impact factor: 5.958
Authors: L-W Chen; M-T Tint; M V Fortier; I M Aris; L P-C Shek; K H Tan; S-Y Chan; P D Gluckman; Y-S Chong; K M Godfrey; V S Rajadurai; F Yap; M S Kramer; Y S Lee Journal: Int J Obes (Lond) Date: 2017-10-09 Impact factor: 5.095
Authors: Rodrigo A Lima; Gernot Desoye; David Simmons; Roland Devlieger; Sander Galjaard; Rosa Corcoy; Juan M Adelantado; Fidelma Dunne; Jürgen Harreiter; Alexandra Kautzky-Willer; Peter Damm; Elisabeth R Mathiesen; Dorte M Jensen; Lise-Lotte T Andersen; Mette Tanvig; Annunziata Lapolla; Maria G Dalfra; Alessandra Bertolotto; Urszula Manta; Ewa Wender-Ozegowska; Agnieszka Zawiejska; David J Hill; Frank J Snoek; Judith G M Jelsma; Mireille van Poppel Journal: Paediatr Perinat Epidemiol Date: 2020-04-30 Impact factor: 3.980