81 research outputs found

    Maternal milk consumption, fetal growth, and the risks of neonatal complications: The Generation R Study

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    Background: Maternal cow-milk consumption may increase birth weight. Previous studies did not assess the association of maternal milk consumption with trimester-specific fetal growth. Objective: The objective was to assess associations of first-trimester maternal milk consumption with fetal growth characteristics in different trimesters and the risk of neonatal complications. Design: In total, 3405 mothers participating in a prospective cohort study completed a 293-item semiquantitative food-frequency questionnaire to obtain information about dairy consumption during the first trimester of pregnancy. Fetal head circumference, femur length, and weight were estimated in the second and third trimesters by ultrasonography. Results: Maternal milk consumption of >3 glasses/d was associated with greater fetal weight gain in the third trimester of pregnancy, which led to an 88-g (95% CI: 39, 135 g) higher birth weight than that with milk consumption of 0 to 1 glass/d. In addition, head circumference tended to be 2.3 cm (95% CI: -0.0, 4.6 cm) larger when mothers consumed >3 glasses/d. Maternal milk consumption was not associated with length growth. Maternal protein intake (P for trend = 0.01), but not fat or carbohydrate intake, from dairy products was associated with higher birth weight. This association appeared to be limited to milk (P for trend < 0.01), whereas protein intake from nondairy food or cheese was not associated with birth weight. Conclusions: Maternal milk consumption is associated with greater fetal weight gain. The association seems to be due to milk protein, or milk components closely associated with protein, rather than to the fat or carbohydrate fraction of milk

    Determination of the primary structure and carboxyl pKAs of heparin-derived oligosaccharides by band-selective homonuclear-decoupled two-dimensional 1H NMR

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    Determination of the structure of heparin-derived oligosaccharides by 1H NMR is challenging because resonances for all but the anomeric protons cover less than 2 ppm. By taking advantage of increased dispersion of resonances for the anomeric H1 protons at low pD and the superior resolution of band-selective, homonuclear-decoupled (BASHD) two-dimensional 1H NMR, the primary structure of the heparin-derived octasaccharide ∆UA(2S)-[(1 → 4)-GlcNS(6S)-(1 → 4)-IdoA(2S)-]3-(1 → 4)-GlcNS(6S) has been determined, where ∆UA(2S) is 2-O-sulfated ∆4,5-unsaturated uronic acid, GlcNS(6S) is 6-O-sulfated, N-sulfated β-d-glucosamine and IdoA(2S) is 2-O-sulfated α-l-iduronic acid. The spectrum was assigned, and the sites of N- and O-sulfation and the conformation of each uronic acid residue were established, with chemical shift data obtained from BASHD-TOCSY spectra, while the sequence of the monosaccharide residues in the octasaccharide was determined from inter-residue NOEs in BASHD-NOESY spectra. Acid dissociation constants were determined for each carboxylic acid group of the octasaccharide, as well as for related tetra- and hexasaccharides, from chemical shift–pD titration curves. Chemical shift–pD titration curves were obtained for each carboxylic acid group from sub-spectra taken from BASHD-TOCSY spectra that were measured as a function of pD. The pKAs of the carboxylic acid groups of the ∆UA(2S) residues are less than those of the IdoA(2S) residues, and the pKAs of the carboxylic acid groups of the IdoA(2S) residues for a given oligosaccharide are similar in magnitude. Relative acidities of the carboxylic acid groups of each oligosaccharide were calculated from chemical shift data by a pH-independent method

    Milk feeding, solid feeding, and obesity risk:a review of the relationships between early life feeding practices and later adiposity

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    Childhood obesity is a major health issue with associated ill-health consequences during childhood and into later adolescence and adulthood. Given that eating behaviors are formed during early childhood, it is important to evaluate the relationships between early life feeding practices and later child adiposity. This review describes and evaluates recent literature exploring associations between child weight and the mode of milk feeding, the age of introducing solid foods and caregivers’ solid feeding practices. There are many inconsistencies in the literature linking early life feeding to later obesity risk and discrepancies may be related to inconsistent definitions, or a lack of control for confounding variables. This review summarizes the literature in this area and identifies the need for large scale longitudinal studies to effectively explore how early life feeding experiences may interact with each other and with nutritional provision during later childhood to predict obesity risk

    Effect of growth in infancy on body composition, insulin resistance, and concentration of appetite hormones in adolescence

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    Background: High infancy weight gain is associated with increased body mass index (BMI) and insulin resistance (IR) in later life, but the association with later body composition has not been well ex-plored. Appetite regulatory hormones may be programmed in early life, but data to support this are lacking. Objective: We investigated the effect of weight gain in infancy on body composition, IR, leptin, ghrelin, and adiponectin at 17 y of age. Design: This was an observational study of 95 term and appropri-ate-for-gestational-age infants. We measured weight at birth and 9 mo of age and, for a subgroup (n = 60), at 3 and 6 mo of age. Changes in weight SD scores from 0 to 9, 0 to 3, 3 to 6, and 6 to 9 mo of age were calculated. Follow-up examinations at 10 and 17 y of age included body fat (BF) assessment by dual-energy X-ray absorptiometry scanning. We measured serum leptin, ghrelin adipo-nectin, and IR at 17 y of age. Results: Weight gain from 0 to 9 mo of age was positively associ-ated with BMI (P, 0.003), percentage BF (P, 0.05), and per-centage trunk fat (TF) (P, 0.03) but not with percentage of TF fat relative to total BF, in childhood and adolescence, and most of these effects were explained by growth from 0 to 3 mo of age. Weight gains from 0 to 9 and 0 to 3 mo of age were not related to IR or leptin but were negatively associated with ghrelin and adiponectin corrected for BF at 17 y of age. Conclusion: Our findings suggest that high weight gain in infancy, especially from 0 to 3 mo of age, has a role in programming both BF and concentrations of ghrelin and adiponectin in adolescence, whereas there was no effect on IR or leptin in this study. Am J Clin Nutr doi: 10.3945/ajcn.2009.27956
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