The importance of maternal insulin resistance throughout pregnancy on neonatal adiposity.
endocrinology
gynaecology
insulin
lipid metabolism
obesity
Journal
Paediatric and perinatal epidemiology
ISSN: 1365-3016
Titre abrégé: Paediatr Perinat Epidemiol
Pays: England
ID NLM: 8709766
Informations de publication
Date de publication:
01 2021
01 2021
Historique:
received:
18
01
2020
revised:
21
03
2020
accepted:
24
03
2020
pubmed:
1
5
2020
medline:
25
11
2021
entrez:
1
5
2020
Statut:
ppublish
Résumé
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. 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. 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. 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). 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.
Sections du résumé
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.
Identifiants
pubmed: 32352590
doi: 10.1111/ppe.12682
pmc: PMC7891448
doi:
Substances chimiques
Triglycerides
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
83-91Subventions
Organisme : Department of Health
Pays : United Kingdom
Informations de copyright
© 2020 The Authors. Paediatric and Perinatal Epidemiology published by John Wiley & Sons Ltd.
Références
Int J Obes (Lond). 2006 Jul;30(7):1056-61
pubmed: 16801943
Am J Obstet Gynecol. 2006 Oct;195(4):1100-3
pubmed: 16875645
Diabet Med. 2011 Sep;28(9):1053-9
pubmed: 21658120
N Engl J Med. 2013 Dec 5;369(23):2173-5
pubmed: 24224559
Hum Reprod. 1993 Oct;8(10):1550-5
pubmed: 8300805
Nutrients. 2015 Jul 10;7(7):5615-27
pubmed: 26184296
PLoS One. 2013;8(2):e57467
pubmed: 23460863
J Clin Endocrinol Metab. 2015 Apr;100(4):1672-80
pubmed: 25574704
Diabet Med. 2018 Oct;35(10):1425-1433
pubmed: 29766563
Int J Obes (Lond). 2018 Mar;42(3):501-506
pubmed: 28990589
Diabetes. 2009 Feb;58(2):453-9
pubmed: 19011170
J Clin Endocrinol Metab. 2014 Jan;99(1):240-7
pubmed: 24243635
BMC Pregnancy Childbirth. 2013 Jul 05;13:142
pubmed: 23829946
Diabetes Care. 2016 Jun;39(6):982-7
pubmed: 27208333
Am J Hum Biol. 2003 Sep-Oct;15(5):667-80
pubmed: 12953179
Diabetes Care. 2019 Aug;42(8):1380-1389
pubmed: 31182492
Diabetes Care. 2011 Oct;34(10):2198-204
pubmed: 21775754
Nord Med. 1952 Jul 25;47(30):1049
pubmed: 14948109
Diabetes Care. 2012 Mar;35(3):574-80
pubmed: 22301123
Clin Ther. 2018 Oct;40(10):1638-1647
pubmed: 30236792
Am J Clin Nutr. 2002 Nov;76(5):1096-100
pubmed: 12399284
Diabetologia. 2015 May;58(5):937-41
pubmed: 25628236
Diabetologia. 2019 Jun;62(6):915-925
pubmed: 30840112
Lancet. 2014 Aug 30;384(9945):766-81
pubmed: 24880830
Am J Hum Biol. 2010 May-Jun;22(3):330-5
pubmed: 19844898
Am J Clin Nutr. 2015 Feb;101(2):302-9
pubmed: 25646327
PLoS One. 2018 Aug 9;13(8):e0202183
pubmed: 30092099
JAMA. 2017 Jun 6;317(21):2207-2225
pubmed: 28586887
JAMA. 2018 Sep 11;320(10):1005-1016
pubmed: 30208453
Paediatr Perinat Epidemiol. 2021 Jan;35(1):83-91
pubmed: 32352590
Pediatr Obes. 2020 Jul;15(7):e12628
pubmed: 32141687
Diabetologia. 1985 Jul;28(7):412-9
pubmed: 3899825
PLoS One. 2017 Jul 27;12(7):e0181307
pubmed: 28750045
Acta Obstet Gynecol Scand. 2015 Aug;94(8):852-60
pubmed: 25912426
Diabetologia. 2019 Apr;62(4):598-610
pubmed: 30648193