Abstract

Gestational weight gain (GWG) is an important modifiable factor known to influence fetal outcomes including birth weight and adiposity. Unlike behaviors such as smoking and alcohol consumption, the effect of GWG throughout pregnancy on fetal development and other outcomes has not been extensively studied. The aim of this study was to investigate the relationship of GWG with endocrine factors such as adiponectin, leptin, and C-reactive protein which may be associated with inflammatory response, fetal growth, and adiposity later in life. Data were obtained from the Ulm Birth Cohort Study (UBCS) and the Ulm SPATZ Health Study, two methodologically similar birth cohort studies including newborns and their mothers recruited from 11/2000–11/2001 and 04/2012–05/2013. In the two included birth cohorts we consistently observed statistically significant positive associations between GWG beginning as early as the second trimester with fetal cord blood leptin and stronger association beginning as early as the first trimester with post-delivery maternal serum leptin. Total weight gain exceeding commonly accepted recommended guidelines was consistently associated with higher leptin levels in both cord blood and post-delivery maternal serum. These results suggest a potential pathomechanistic link between fetal environment and surrogate markers of long-term health.

Highlights

  • Mounting evidence suggests fetal environment and nutrition may play a role in the origin of a number of chronic diseases manifesting later in life[1]

  • Total weight gained by obese mothers was significantly lower in SPATZ than in Ulm Birth Cohort Study (UBCS) and less likely to be classified as excessive (p = 0.02)

  • In our analyses of two birth cohorts recruited from the general population with identical sampling and measurement methodologies and a time lag of 11 years, we observed significant positive association between Gestational weight gain (GWG) beginning as early as the second trimester and cord blood leptin

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Summary

Introduction

Mounting evidence suggests fetal environment and nutrition may play a role in the origin of a number of chronic diseases manifesting later in life[1]. Though a number of confounding factors such as offspring gender, parity, and smoking are known to influence fetal growth[5,6], fetal resource availability is primarily associated with maternal size and body composition, dietary intake, and placental function[7,8] In relation to these factors, one large scale retrospective study comparing successive births within mothers identified overall gestational weight gain (GWG) as a contributing factor to birthweight[9]. Several studies have reported positive correlations between cord blood adiponectin and leptin levels and either birthweight or size for gestational age[16,17,18], as well as, body mass index (BMI) in children up to 3 years of age[19,20] These results suggest fetally programmed adipokine levels may play a role as a potential biological mechanism for such associations, but require further refined analyses and corroboration in independent cohorts. In contrast to previous studies which have only reported associations observed with either cord blood or maternal serum levels of each biomarker, fetal and maternal outcomes were directly compared in order to explore potential pathomechanistic associations

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