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1.
J Pediatr ; 201: 27-33.e4, 2018 10.
Article in English | MEDLINE | ID: mdl-30007772

ABSTRACT

OBJECTIVE: To examine whether feeding patterns from birth to age 6 months modify the association between birth weight and weight at 7-12 months of age. STUDY DESIGN: Longitudinal mixed models were used to examine feeding trajectories across categories of birth weight and weight at 7-12 months of age in 1799 mother-infant dyads enrolled in the Infant Feeding Practices Study II. The percentage of breast milk received and the average daily formula consumption were calculated from birth to 6 months of age. Birth weights were classified as high (≥4000 g) and normal (≥2500 g and <4000 g). Weights at 7-12 months of age were categorized as high (z score >1) or normal (z score ≤1). A secondary analysis was performed using categories defined by birth weight adjusted for gestational age percentiles (>90% and 10th-90th percentile). RESULTS: High birth weight (HBW) infants with high weights at 7-12 months of age demonstrated a rapid decline in the percentage of breast milk feedings compared with HBW infants with normal weights at 7-12 months of age. Normal birth weight infants with high weights at 7-12 months of age received a lower percentage of breast milk and had greater absolute intakes of formula than those with normal weights at 7-12 months of age; these associations did not vary over time. Results were similar when infants were categorized by birth weight percentiles. CONCLUSIONS: A lower proportion of breast milk feedings was associated with excess weight at 7-12 months of age in HBW infants. These findings suggest an initial target for obesity prevention programs focusing on the first 6 months after birth.


Subject(s)
Birth Weight , Breast Feeding/statistics & numerical data , Weight Gain , Adult , Female , Humans , Infant , Infant Formula/statistics & numerical data , Infant Nutritional Physiological Phenomena , Infant, Newborn , Linear Models , Longitudinal Studies , Male , Pediatric Obesity/prevention & control , Surveys and Questionnaires
2.
Early Hum Dev ; 90(10): 545-8, 2014 Oct.
Article in English | MEDLINE | ID: mdl-25103788

ABSTRACT

BACKGROUND: High birth weight (HBW) is considered a key predictor of the development of chronic diseases, such as Type 2 Diabetes (T2D). Foetal growth depends on many factors, among which placental function is critical. Some genes with expression in the placenta, such as GRB10, are known to be involved in the regulation of insulin receptor pathways and the size of mouse littermates. AIM: To evaluate whether the intronic polymorphism rs12540874 A>G of the GRB10 gene is associated with HBW in term newborns. STUDY DESIGN: A total of 51 healthy term newborns were enrolled in a nested case-control study. The case group was defined by the presence of HBW (n=17) and the control group by newborns with normal birth weight (NBW n=34). Maternal and foetal factors influencing HBW were considered as exclusion criteria. The polymorphism was determined through real-time PCR using TaqMan technology. Categorical variables were evaluated with descriptive statistics, and multivariate logistic regression analysis was used to evaluate the association between polymorphism and HBW. RESULTS: The newborns in the case group had a longer gestation period (39. 7 ± 1.0 and 38.8 ± 1.8 weeks) and higher insulin levels at birth (9.5 ± 4.0 and 5.7 ± 3.4 µU/mL) than the newborns in the control group. The multivariate regression analysis, adjusted for weeks of gestation, showed a significant association between the SNP rs12540874 A>G of the GRB10 gene with HBW (OR 4.9; CI95% 1.10-22.10 p=0.02). CONCLUSIONS: Our results suggest that the SNP rs12540874 A>G, an intronic SNP of the gene GRB10, is associated with HBW.


Subject(s)
Birth Weight/genetics , Fetal Diseases/genetics , GRB10 Adaptor Protein/genetics , Gene Expression Regulation, Developmental/genetics , Hyperinsulinism/genetics , Polymorphism, Single Nucleotide/genetics , Case-Control Studies , Humans , Infant, Newborn , Insulin/metabolism , Logistic Models , Real-Time Polymerase Chain Reaction , Signal Transduction/genetics
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