Abstract

Women with pre-gestational diabetes have a high rate of large for gestational age (LGA) babies compared to women without diabetes. In particular, there is a high rate of asymmetric LGA defined as ponderal index (PI) > 90th percentile for gestational age. We examined the association of birth weight and PI, with body mass index (BMI) and obesity status in adulthood, in a cohort of offspring of women with pre-gestational diabetes. The women participated in the Diabetes in Pregnancy (DiP) study at the University of Cincinnati from 1978 to 1995. The offspring of these women are the cohort participating in an observational study being conducted at Cincinnati Children’s Hospital Medical Center. Once located, the offspring were invited to come in for a one-day clinic visit to assess anthropometrics, and their metabolic, renal and cardiovascular status. Linear and logistic regression was used to assess the association between birth weight and PI with current BMI. We report on 107 offspring. A statistically significant association was found between offspring current BMI with birth PI (β = 1.89, 95% CI 0.40–3.38), and between offspring current obesity status and birth asymmetric LGA (aOR = 2.44, 95% CI 1.01–5.82). This is consistent with in utero “metabolic programming”.

Highlights

  • For those with pre-gestational diabetes, the associated exacerbations and fluctuations of glucose in utero have been shown to be independently associated with infant birthweight [1]

  • Leveraging data from an ongoing observational study, we examined preliminary outcome data describing the obesity status from our first 107 study participants who were young adult offspring of women who participated in the Diabetes in Pregnancy (DiP) study between 1978 and 1995

  • At birth the offspring had a mean weight of 3345 g, ponderal index (PI) 2.96 g/cm3, and 27% were asymmetric large for gestational age (LGA) and 49% LGA

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Summary

Introduction

For those with pre-gestational diabetes, the associated exacerbations and fluctuations of glucose in utero have been shown to be independently associated with infant birthweight [1]. Despite the exponential improvements in diabetes control in recent decades, the rate of LGA babies born to women with pre-gestational diabetes has not decreased [2,3]. This apparent paradox may be due to the increased insulin taken to aid glycemic control in the mother, which crosses the placenta and acts as a growth factor for the fetus [4]. The maternal glucose crossing the placenta acts as a growth factor by stimulating the production of fetal insulin via the fetal pancreas, which is active as early as 20 weeks’ gestation [5,6]. We and others have demonstrated that this “fat” baby is subject to increased risk for other morbidities at delivery, such as hypoglycemia, hyperbilirubinemia and acidosis [7,8], where this “fat” baby is defined as asymmetrically LGA, i.e., LGA for weight but not LGA for length, or LGA for ponderal index (PI)

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