Abstract

BackgroundMaternal obesity and gestational diabetes mellitus (GDM) may independently influence offspring fat mass and metabolic disease susceptibility. In this pilot study, body composition and fat distribution in offspring from obese women with and without GDM and lean women were assessed within the 1st year of life, and maternal and newborn plasma factors were related to offspring adipose tissue distribution.MethodsSerum and plasma samples from pregnant obese women with (n = 16) or without (n = 13) GDM and normoglycemic lean women (n = 15) at 3rd trimester and offspring cord plasma were used for analyzing lipid profiles, insulin and adipokine levels. At week-1 and 6, month-4 and year-1, offspring anthropometrics and skinfold thickness (SFT) were measured and abdominal subcutaneous (SCA) and preperitoneal adipose tissue (PPA) were determined by ultrasonography.ResultsCord insulin was significantly increased in the GDM group, whereas levels of cord leptin, total and high molecular weight (HMW) adiponectin were similar between the groups. Neonates of the GDM group showed significantly higher SFT and fat mass until week-6 and significantly increased SCA at week-1 compared to the lean group that persisted as strong trend at week-6. Interestingly, PPA in neonates of the GDM group was significantly elevated at week-1 compared to both the lean and obese group. At month-4 and year-1, significant differences in adipose tissue growth between the groups were not observed. Multiple linear regression analyses revealed that cord insulin levels are independently related to neonatal PPA that showed significant relation to PPA development at year-1. Maternal fasted C-peptide and HMW adiponectin levels at 3rd trimester emerged to be determinants for PPA at week-1.ConclusionMaternal pregravid obesity combined with GDM leads to newborn hyperinsulinemia and increased offspring fat mass until week-6, whereas pregravid obesity without GDM does not. This strongly suggests the pivotal role of GDM in the adverse offspring outcome. Maternal C-peptide and HMW adiponectin levels in pregnancy emerge to be predictive for elevated PPA in newborns and might be indicative for the obesity risk at later life. Altogether, the findings from our pilot study warrant evaluation in long-term studies.Trial registrationGerman Clinical Trials Register DRKS00004370

Highlights

  • Maternal obesity and gestational diabetes mellitus (GDM) may independently influence offspring fat mass and metabolic disease susceptibility

  • Maternal C-peptide and high molecular weight (HMW) adiponectin levels in pregnancy emerge to be predictive for elevated preperitoneal adipose tissue (PPA) in newborns and might be indicative for the obesity risk at later life

  • We found that obese mothers, characterized by hyperinsulinemia and increased Homeostasis model of assessment-insulin resistance (HOMA-IR)-index, had decreased HMW adiponectin and HMW-total adiponectin ratio (SA) which is in line with recent data from animal and clinical studies reporting that insulin is a negative regulator of adiponectin, preferentially HMW oligomer, secretion [55]

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Summary

Introduction

Maternal obesity and gestational diabetes mellitus (GDM) may independently influence offspring fat mass and metabolic disease susceptibility. In this pilot study, body composition and fat distribution in offspring from obese women with and without GDM and lean women were assessed within the 1st year of life, and maternal and newborn plasma factors were related to offspring adipose tissue distribution. Besides maternal age, ethnicity and family history of diabetes, a major predictor for gestational diabetes mellitus (GDM) [5]. Maternal obesity and GDM are independent risk factors for fetal hyperinsulinemia, elevated weight and body fat at birth, suggesting that both GDM and pregravid obesity influence fetal development through similar mechanism [6,7,8]. Children born from obese and/or diabetic mothers are at higher risk for obesity and insulin resistance/ type 2 diabetes from childhood periods [9,10,11] and adolescence [11,12] up to adulthood [13,14]

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