Eleanor M Jarvie 1 , Frances M Stewart 2 , Jane E Ramsay 2 , E Ann Brown 2 , Barbara J Meyer 3 , Gunilla Olivecrona 4 , Bruce A Griffin 5 , Dilys J Freeman 1 . Show Affiliations »
Abstract
CONTEXT: Maternal body mass index (BMI) is associated with increased birth weight but does not explain all the variance in fetal adiposity. OBJECTIVE: To assess the contribution of maternal body fat distribution to offspring birth weight and adiposity. DESIGN: Longitudinal study throughout gestation and at delivery. SETTING: Women recruited at 12 weeks of gestation and followed up at 26 and 36 weeks. Cord blood was collected at delivery. PATIENTS: Pregnant women (n = 45) with BMI 18.0 to 46.3 kg/m2 and healthy pregnancy outcome. METHODS: Maternal first trimester abdominal subcutaneous and visceral adipose tissue thickness (SAT and VAT) was assessed by ultrasound. MAIN OUTCOME MEASURES: Maternal body fat distribution, maternal and cord plasma glucose and lipid concentrations, placental weight, birth weight, and fetal adiposity assessed by cord blood leptin. RESULTS: VAT was the only anthropometric measure independently associated with birth weight centile (r2 adjusted 15.8%, P = .002). BMI was associated with trimester 2 and trimesters 1 through 3 area under the curve (AUC) glucose and insulin resistance (Homeostatic Model Assessment). SAT alone predicted trimester 2 lipoprotein lipase (LPL) mass (a marker of adipocyte insulin sensitivity) (11.3%, P = .017). VAT was associated with fetal triglyceride (9.3%, P = .047). Placental weight was the only independent predictor of fetal adiposity (48%, P < .001). Maternal trimester 2 and AUC LPL were inversely associated with fetal adiposity (r = -0.69, P = .001 and r = -0.58, P = .006, respectively). CONCLUSIONS: Maternal VAT provides additional information to BMI for prediction of birth weight. VAT may be a marker of reduced SAT expansion and increased availability of maternal fatty acids for placental transport. © Endocrine Society 2019. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.
CONTEXT: Maternal body mass index (BMI) is associated with increased birth weight but does not explain all the variance in fetal adiposity. OBJECTIVE: To assess the contribution of maternal body fat distribution to offspring birth weight and adiposity. DESIGN: Longitudinal study throughout gestation and at delivery. SETTING: Women recruited at 12 weeks of gestation and followed up at 26 and 36 weeks. Cord blood was collected at delivery. PATIENTS : Pregnant women (n = 45) with BMI 18.0 to 46.3 kg/m2 and healthy pregnancy outcome. METHODS: Maternal first trimester abdominal subcutaneous and visceral adipose tissue thickness (SAT and VAT) was assessed by ultrasound. MAIN OUTCOME MEASURES: Maternal body fat distribution, maternal and cord plasma glucose and lipid concentrations, placental weight, birth weight, and fetal adiposity assessed by cord blood leptin . RESULTS: VAT was the only anthropometric measure independently associated with birth weight centile (r2 adjusted 15.8%, P = .002). BMI was associated with trimester 2 and trimesters 1 through 3 area under the curve (AUC) glucose and insulin resistance (Homeostatic Model Assessment). SAT alone predicted trimester 2 lipoprotein lipase (LPL ) mass (a marker of adipocyte insulin sensitivity) (11.3%, P = .017). VAT was associated with fetal triglyceride (9.3%, P = .047). Placental weight was the only independent predictor of fetal adiposity (48%, P < .001). Maternal trimester 2 and AUC LPL were inversely associated with fetal adiposity (r = -0.69, P = .001 and r = -0.58, P = .006, respectively). CONCLUSIONS: Maternal VAT provides additional information to BMI for prediction of birth weight. VAT may be a marker of reduced SAT expansion and increased availability of maternal fatty acids for placental transport. © Endocrine Society 2019. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.
Entities: Chemical
Gene
Species
Keywords:
Adipose tissue; Birth weight; Body fat distribution; Insulin resistance; Pregnancy
Year: 2020
PMID: 31832635 DOI: 10.1210/clinem/dgz248
Source DB: PubMed Journal: J Clin Endocrinol Metab ISSN: 0021-972X Impact factor: 5.958