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      Birth Weight and Long-Term Metabolic Outcomes: Does the Definition of Smallness Matter?

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          Objective: To establish the role of individual definition of smallness at birth in the association between birth weight and long-term metabolic outcomes. Methods: Lipid profile and oral glucose tolerance test were performed in young adults (22 years) born either small (SGA) or appropriate for gestational age (AGA). AGA/SGA were defined by both population-based and customized methods adjusting for individual maternal/pregnancy characteristics. 825 individuals were classified as AGA and 575 as SGA by both methods, 131 were SGA by the population-based method only (SGA<sub>pop</sub>) and 22 were SGA by the customized method only (SGA<sub>cust</sub>). Results: SGA<sub>cust</sub> subjects had higher total cholesterol and triglyceride levels and lower high-density lipoprotein cholesterol concentrations than SGA<sub>pop</sub> and AGA subjects, however, insignificantly when adjusted for age, gender and body mass index. The homeostasis model assessment for insulin resistance (HOMA-IR) index was higher in the SGA<sub>cust</sub> (p = 0.05) and SGA<sub>pop</sub> (p = 0.02) versus the AGA group. Controlling for the HOMA-IR index, the insulinogenic index was significantly lower in the SGA<sub>cust</sub> versus SGA<sub>pop</sub> (p = 0.001) and AGA (p = 0.003) groups. In SGA<sub>cust</sub> individuals, the HOMA-IR index was clearly shifted to higher, while the insulinogenic index to lower tertiles of AGA distribution; SGA<sub>pop</sub> subjects had the HOMA-IR and insulinogenic index predominantly in the highest tertiles. Conclusions: Individualized birth weight standards allow to better identify subjects who failed to reach their genetic potential of intrauterine growth and are at higher risk of metabolic disturbances and impaired insulin secretion later in life.

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          Most cited references 11

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          Birth weight and non-insulin dependent diabetes: thrifty genotype, thrifty phenotype, or surviving small baby genotype?

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            Dynamic change in adiposity from fetal to postnatal life is involved in the metabolic syndrome associated with reduced fetal growth.

            The aims of this study were to establish the role of insulin resistance in the metabolic syndrome associated with restricted fetal growth and to characterise the fetal and postnatal determinants responsible for the long-term metabolic outcome. The study population consisted of adults selected on birth data from a maternity registry and born either small for gestational age (SGA) (n=734, birthweight
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              Beta-cell mass and proliferation following late fetal and early postnatal malnutrition in the rat.

              We have recently shown that maternal food restriction during late pregnancy in rats decreased beta-cell mass in the offspring at birth, without altering beta-cell proliferation. The aim of the present work was to determine: 1) whether sustained maternal undernutrition until weaning (R group) more dramatically alters beta-cell mass in the offspring and if normal food supply from weaning until adulthood could reverse the deleterious effects and; 2) if altered beta-cell proliferation was responsible for the decreased beta-cell mass. Beta-cell fraction and proliferative capacity were determined during the suckling period and at adult age after ad libitum feeding from weaning in the R animals and in age-matched controls (C group). At day 21, the offspring born and nursed by food-restricted mothers (R animals) showed a 66% reduction in beta-cell mass and number, which did not increase from birth to weaning, although beta-cell proliferation remained normal. At 3 months of age, R animals had 35% decreased beta-cell fraction, with a 50% decrease in the head of the pancreas. In that area, beta-cell proliferation was similar to that of the controls. In the tail of the pancreas, beta-cell fraction was only slightly impaired but beta-cell proliferation was increased by 37%, as compared with the controls. This increase was associated with a shift in islet size distribution towards medium and large islets compared with the head of pancreas from these R animals. No regional variations of beta-cell fraction, proliferation or islet size distribution were observed in adult control animals. In conclusion, prolonged malnutrition until weaning impairs beta-cell development but not beta-cell proliferation. Subsequent re-nutrition is followed by increased beta-cell proliferation but this is insufficient to fully restore beta-cell mass.

                Author and article information

                Horm Res Paediatr
                Hormone Research in Paediatrics
                S. Karger AG
                November 2008
                30 September 2008
                : 70
                : 5
                : 309-315
                aINSERM, Unité 690 and bService de biochimie et d’hormonologie, Hôpital Robert Debré, Paris, France; cWest Midlands Perinatal Institute, Birmingham, UK
                157878 Horm Res 2008;70:309–315
                © 2008 S. Karger AG, Basel

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                Page count
                Figures: 2, Tables: 2, References: 21, Pages: 7
                Original Paper


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