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      Hyperglycemia and Adverse Pregnancy Outcome (HAPO) Study : Associations With Neonatal Anthropometrics

      research-article
      The HAPO Study Cooperative Research Group *
      Diabetes
      American Diabetes Association

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          Abstract

          OBJECTIVE—To examine associations of neonatal adiposity with maternal glucose levels and cord serum C-peptide in a multicenter multinational study, the Hyperglycemia and Adverse Pregnancy Outcome (HAPO) Study, thereby assessing the Pederson hypothesis linking maternal glycemia and fetal hyperinsulinemia to neonatal adiposity.

          RESEARCH DESIGN AND METHODS—Eligible pregnant women underwent a standard 75-g oral glucose tolerance test between 24 and 32 weeks gestation (as close to 28 weeks as possible). Neonatal anthropometrics and cord serum C-peptide were measured. Associations of maternal glucose and cord serum C-peptide with neonatal adiposity (sum of skin folds >90th percentile or percent body fat >90th percentile) were assessed using multiple logistic regression analyses, with adjustment for potential confounders, including maternal age, parity, BMI, mean arterial pressure, height, gestational age at delivery, and the baby's sex.

          RESULTS—Among 23,316 HAPO Study participants with glucose levels blinded to caregivers, cord serum C-peptide results were available for 19,885 babies and skin fold measurements for 19,389. For measures of neonatal adiposity, there were strong statistically significant gradients across increasing levels of maternal glucose and cord serum C-peptide, which persisted after adjustment for potential confounders. In fully adjusted continuous variable models, odds ratios ranged from 1.35 to 1.44 for the two measures of adiposity for fasting, 1-h, and 2-h plasma glucose higher by 1 SD.

          CONCLUSIONS—These findings confirm the link between maternal glucose and neonatal adiposity and suggest that the relationship is mediated by fetal insulin production and that the Pedersen hypothesis describes a basic biological relationship influencing fetal growth.

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          Most cited references12

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          Diabetes

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            Anthropometric estimation of neonatal body composition.

            (1995)
            Estimation of neonatal body composition can be useful in the understanding of fetal growth. However, body composition methods such as total body water and total body electric conductivity are expensive and not readily available. Our primary purpose was to develop an anthropometric model to estimate neonatal body composition and prospectively validate the model against total body electric conductivity and secondarily to compare our anthropometric model and a previously published anthropometric formula with total body electric conductivity. A total of 194 neonates had estimates of body composition according to total body electric conductivity (group 1). Parental morphometrics, gestational age, race, sex, parity, and neonatal measurements including birth weight, length, head circumference, and skinfolds (triceps, subscapular, flank, and thigh) were correlated with body fat by use of stepwise regression analysis. The model was validated in a second group of 65 neonates (group 2). There were no significant differences in any of the parental or neonatal measurements between groups 1 and 2. In group 1, 78% of the variance in body fat with the use of total body electric conductivity was explained by birth weight, length, and flank skinfold (R2 = 0.78, p = 0.0001). When prospectively validated by the subjects in group 2, the model had significant and stronger correlation (R2 = 0.84, p = 0.0001) with body fat estimated by total body electric conductivity as compared with the other anthropometric model (R2 = 0.54, p = 0.0001). There was no significant (p = 0.11) difference between our anthropometric estimate of body fat and total body electric conductivity. The anthropometric model developed can be used to reasonably predict neonatal body fat mass at birth.
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              Obesity in pregnancy.

              Overweight and obesity are common findings in women of reproductive age in the UK; as 32% of 35- to 64-year-old women are overweight and 21% obese. Obesity causes major changes in many features of maternal intermediary metabolism. Insulin resistance appears to be central to these changes and may also be involved in increased energy accumulation by the fetus. Maternal obesity is associated with many risks to the pregnancy, with increased risk of miscarriage (three-fold) and operative delivery (20.7 versus 33.8% in the obese and 47.4% in the morbidly obese group). Other risks to the mother include an increased risk of pre-eclampsia (3.9 versus 13.5% in the obese group) and thromboembolism (0.05 versus 0.12% in the obese group). There are risks to the fetus with increased perinatal mortality (1.4 per 1000 versus 5.7 per 1000 in the obese group) and macrosomia (>90th centile; 9 versus 17.5% in the obese group). Maternal obesity is associated with an increased risk of obesity in the long term. Obese woman should try to lose weight before pregnancy but probably not during pregnancy. There is no real evidence base for the management of maternal obesity but some practical suggestions are made.
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                Author and article information

                Journal
                Diabetes
                diabetes
                Diabetes
                American Diabetes Association
                0012-1797
                1939-327X
                February 2009
                : 58
                : 2
                : 453-459
                Author notes
                [*]

                A complete list of members of the HAPO Study Cooperative Research Group is included in the appendix of the following article: HAPO Study Cooperative Research Group: Hyperglycemia and adverse pregnancy outcomes. N Engl J Med 358:1991–2002, 2008.

                Corresponding author: Boyd E. Metzger, bem@ 123456northwestern.edu

                Article
                582453
                10.2337/db08-1112
                2628620
                19011170
                ab89f790-3be2-4266-ba0c-610ccc2101fc
                Copyright © 2009, American Diabetes Association

                Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.

                History
                : 14 August 2008
                : 11 November 2008
                Categories
                Pathophysiology

                Endocrinology & Diabetes
                Endocrinology & Diabetes

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