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The Impact of Maternal Glycemia and Obesity on Early Postnatal Growth in a Nondiabetic Caucasian Population

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The Impact of Maternal Glycemia and Obesity on Early Postnatal Growth in a Nondiabetic Caucasian Population Clinical Care/Education/Nutrition ORIGINAL ARTICLE The Impact of Maternal Glycemia and Obesity on Early Postnatal Growth in a Nondiabetic Caucasian Population 1,2 3 BRIDGET KNIGHT, PHD ROY J. POWELL, PHD reflects maternal glycemia, with birth 1 4 BEVERLEY M. SHIELDS, PHD DAVID WRIGHT, PHD weight being increased in diabetic preg- 1 1 ANITA HILL ANDREW T. HATTERSLEY, DM nancies, and correlates with maternal gly- cemia, in both fasting and stimulated levels, in the nondiabetic pregnancy (15– OBJECTIVE — Offspring of mothers with diabetes have increased birth weight and higher 18). The impact of glycemia within the rates of obesity in early childhood. The relative role of maternal glycemia and maternal obesity normal range on early postnatal growth in is uncertain. We therefore studied the impact of maternal glycemia and maternal obesity on European Caucasians is uncertain. offspring birth measures and early postnatal growth in nondiabetic pregnancies. Studying the effect of maternal gly- cemia on early postnatal growth in the RESEARCH DESIGN AND METHODS — We studied 547 full-term singleton babies of nondiabetic population may give in- nondiabetic parents. Data available included parental height and weight; maternal prepregnant weight; maternal fasting plasma glucose (FPG) at 28 weeks of gestation; and offspring weight and sight into the mechanisms of the effects length at birth, 12 weeks of age, and 1 and 2 years of age. Relationships between parental and seen in the offspring of diabetic moth- offspring measures were estimated using Pearson correlations. ers. We therefore aimed to study the impact of maternal glycemia in the non- RESULTS — Maternal FPG was correlated with offspring birth weight (r ϭ 0.25, P Ͻ diabetic pregnancy and parental BMI on 0.001), length (r ϭ 0.17, P Ͻ 0.001), and BMI (r ϭ 0.2, P Ͻ 0.001) but was not correlated birth measures and early postnatal with offspring growth at 12 weeks. Maternal prepregnancy BMI was significantly correlated growth of offspring. with offspring weight (r ϭ 0.26, P Ͻ 0.001), length (r ϭ 0.12, P ϭ 0.01), and BMI at birth ϭ Ͻ ϭ ϭ (r 0.26, P 0.001) and remained correlated with offspring weight (r 0.13–0.14, P RESEARCH DESIGN AND 0.007–0.002) and BMI (r ϭ 0.14–0.19, P ϭ 0.002 to Ͻ0.001) during the first 2 years. ϭ METHODS Paternal BMI was correlated with offspring weight from 12 weeks onwards (r 0.11–0.22, Ͼ P ϭ 0.017 to Ͻ0.001), length (r ϭ 0.10–0.12, P ϭ 0.01–0.05), and BMI from 1 year We studied 547 full-term (gestation 37 onwards (r ϭ 0.16–0.25, P ϭϽ0.001). weeks) singleton babies and their parents from the Exeter Family Study of Child- CONCLUSIONS — In a nondiabetic cohort, the effect of maternal glycemia on birth weight hood Health (EFSOCH). Subjects with di- is transitory, while the impact on growth of maternal BMI continues into early childhood. The abetes were excluded, and all mothers independent association of paternal BMI with offspring postnatal growth suggests that the had a fasting glucose Ͻ5.5 mmol/l (100 impact of parental BMI could be explained by genetic factors, shared environment, or both. mg/dl) at 28 weeks of gestation. EFSOCH was set up to study fetal and early postna- Diabetes Care 30:777–783, 2007 tal growth by investigating the role of genes and genetic factors within a normal here is strong evidence that the off- in the offspring in early life (14). Possible Caucasian population. This is an ongoing, spring of mothers with prepreg- mechanisms to explain the relative obe- prospective, community-based study T nancy type 2 and gestational sity in early childhood of the offspring in- within a specific area of central Exeter, as diabetes not only have increased birth clude programming by the maternal defined by postcode. The study protocol weight (1–3), but also show increased intrauterine environment, inheriting a ge- has been described in detail previously obesity in childhood and early adult life netic predisposition to obesity, or mater- (19). (2–10). These mothers have an increased nal and childhood obesity representing a Ethics approval was given by the North BMI and are also hyperglycemic (11–13), shared familial environment. and East Devon local ethics committee. both of which may contribute to obesity Insulin-mediated growth of the fetus ●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●●● Data collected 1 2 Height (to nearest 0.1 cm using the Harp- From Peninsula Medical School, Exeter, U.K.; the Maternity Unit, Heavitree Hospital, Royal Devon and enden stadiometer) and weight (to near- Exeter NHS Trust, Exeter, U.K; the 3Research and Development Support Unit, Exeter, U.K.; and the 4School of Mathematics and Statistics, University of Plymouth, Plymouth, U.K. est 0.1 kg using Tanita electric scales) Address correspondence and reprint requests to Professor Andrew T. Hattersley, Diabetes Research, were measured on both parents at 28 Peninsula Medical School, Barrack Road, Exeter, EX2 5AX, U.K. Email: [email protected]. weeks of gestation. All measures were Received for publication 5 September 2006 and accepted in revised form 5 January 2007. taken prospectively by specially trained Published ahead of print at http://care.diabetesjournals.org on 24 January 2007. DOI: 10.2337/dc06- 1849. research midwives. The inter-rater CV be- Abbreviations: EFSOCH, Exeter Family Study of Childhood Health; FPG, fasting plasma glucose; SDS, tween the research midwives for parental SD scores; SES, socio-economic status. weight and height was Ͻ1%. Mother’s A table elsewhere in this issue shows conventional and Syste`me International (SI) units and conversion prepregnant weight was self-reported. factors for many substances. Measurements taken on the offspring at © 2007 by the American Diabetes Association. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby birth, 12 weeks of age, and 1 and 2 years of marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. age include length (to nearest 0.1 cm using DIABETES CARE, VOLUME 30, NUMBER 4, APRIL 2007 777 Parental obesity alters postnatal growth Table 1—Partial correlations of offspring weight, length, and BMI at birth, 12 weeks of age, and 1 and 2 years of age with maternal fasting glucose, maternal prepregnancy BMI, and paternal BMI, corrected for common confounders (sex, gestation, parity, smoking, and socioeconomic status) Weight Length BMI rPrPrP Maternal fasting glucose Birth 0.25 Ͻ0.001 0.17 Ͻ0.001 0.2 Ͻ0.001 12 weeks 0.37 0.40 0.05 0.31 0.02 0.74 1 year Ϫ0.04 0.41 0.01 0.79 Ϫ0.06 0.19 2 years 0.03 0.57 0 0.96 0.03 0.53 Maternal prepregnancy BMI Birth 0.26 Ͻ0.001 0.12 0.01 0.26 Ͻ0.001 12 weeks 0.14 0.002 0.04 0.35 0.14 0.002 1 year 0.13 0.007 Ϫ0.04 0.45 0.19 Ͻ0.001 2 years 0.14 0.004 0.01 0.91 0.17 Ͻ0.001 Paternal BMI Birth 0.06 0.15 0.05 0.27 0.04 0.33 12 weeks 0.11 0.017 0.07 0.11 0.08 0.07 1 year 0.20 Ͻ0.001 0.12 0.01 0.16 Ͻ0.001 2 years 0.22 Ͻ0.001 0.10 0.05 0.25 Ͻ0.001 the Harpenden stadiometer) and weight (to responding parental size to adjust for the Maternal FPG, maternal prepregnancy nearest 0.1 kg using Soehnle scales). Limits effects of assortative mating. Multiple lin- BMI, and paternal BMI tertiles were pro- of agreement (mean Ϯ 2 SD) between the ear regression used SDS to enable com- duced. ANOVA was used to assess signifi- research midwives were within Ϯ 1cmfor parison both between variables and cant differences between the tertiles and all neonatal measures. We used BMI (kg/m2) across time points. child growth measures at each time point. at birth rather than ponderal index to give consistency with postnatal measures. Fasting plasma glucose (FPG) was ob- Table 2—Regression analysis with offspring weight SDS at four time points as the response tained for all mothers at 28 weeks of ges- variables, and maternal FPG, maternal prepregnancy BMI SDS, and paternal BMI SDS as the tation, and the assay was carried out by explanatory variables the pathology laboratories at the Royal Devon & Exeter Hospital, Exeter, U.K. We assigned socio-economic status (SES) Maternal by Townsend Scores based on enumera- Maternal prepregnancy Paternal tion districts by postcode (20). FPG SDS BMI SDS BMI SDS Gestation was calculated from last Birthweight SDS menstrual period in women who had reg- B 0.510 0.038 0.003 ular periods and were confident of the SE 0.118 0.009 0.10 ϭ date of their last period (n 338). Where t 4.31 4.31 0.31 there was doubt about the last menstrual P Ͻ0.001 Ͻ0.001 0.774 period, gestation was calculated by the 12-week weight SDS ϭ “dating scan” (n 209) done early in B Ϫ0.038 0.122 0.075 Ϯ pregnancy (12.6 1.6 weeks) SE 0.048 0.048 0.045 t Ϫ0.78 2.55 1.64 Statistics P 0.435 0.011 0.101 Data were summarized as mean Ϯ SD. SD 1-year weight SDS scores (SDS) were calculated for weight, B Ϫ0.10 0.121 0.182 length, and BMI on all babies at birth, 12 SE 0.050 0.050 0.048 weeks of age, and 1 and 2 years of age.
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