Glucose and Lipid Metabolism in Small-for-Gestational-Age Infants at 72 Hours of Age

Wu, Xinli; Cui, Yun-Pu; Tong, Xiaomei; Ye, Hong-mao; Li, Song

doi:10.1210/jc.2006-1281

Cited by 55 publications

(46 citation statements)

References 28 publications

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“…By contrast, low TG levels found in LGA newborns would be the result of enhanced LPL activity derived from their increased adipose mass. Interestingly, in the pediatric literature there are also reports of high TG levels in the serum of SGA newborns taken a few days after delivery (23,24), especially in infants with a Ponderal index Ͻ10th percentile (24). This fits with our observations and suggests that SGA infants appear to have impaired utilization of circulating TGs, as a consequence of lacking peripheral adipose.…”

Section: Schaefer-graf and Associatessupporting

confidence: 90%

Maternal Lipids as Strong Determinants of Fetal Environment and Growth in Pregnancies With Gestational Diabetes Mellitus

Schaefer-Graf

K²,

Kulbacka³

et al. 2008

Diabetes Care

392

263

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OBJECTIVE -To determine the contribution of maternal glucose and lipids to intrauterine metabolic environment and fetal growth in pregnancies with gestational diabetes mellitus (GDM).RESEARCH DESIGN AND METHODS -In 150 pregnancies, serum triglycerides (TGs), cholesterol, free fatty acids (FFAs), glycerol, insulin, and glucose were determined in maternal serum and cord blood during the 3rd trimester. Maternal glucose values came from oral glucose tolerance testing and glucose profiles. Measurements of fetal abdominal circumference (AC) were performed simultaneously with maternal blood sampling and birth weight, and BMI and neonatal fat mass were obtained following delivery.RESULTS -Maternal TGs and FFAs correlated with fetal AC size (at 28 weeks: triglycerides, P ϭ 0.001; FFAs, P ϭ 0.02), and at delivery they correlated with all neonatal anthropometric measures (FFA: birth weight, P ϭ 0.002; BMI, P ϭ 0.001; fat mass, P ϭ 0.01). After adjustment for confounding variables, maternal FFAs and TGs at delivery remained the only parameters independently related to newborns large for gestational age (LGA) (P ϭ 0.008 and P ϭ 0.04, respectively). Maternal FFA levels were higher in mothers with LGA newborns than in those with appropriate for gestational age (AGA) newborns (362.8 Ϯ 101.7 vs. 252.4 Ϯ 10.1, P ϭ 0.002). Maternal levels of TGs, FFAs, and glycerol at delivery correlated with those in cord blood (P ϭ 0.003, P ϭ 0.004, and P ϭ 0.005, respectively). Fetal triglyceride and cholesterol levels were negatively correlated with newborn birth weight (P ϭ 0.001), BMI (P ϭ 0.004), and fat mass (P ϭ 0.001). TGs were significantly higher in small for gestational age (SGA) newborns compared with AGA or LGA newborns, while insulin-to-glucose ratio and FFAs were the highest in LGA newborns.CONCLUSIONS -In well-controlled GDM pregnancies, maternal lipids are strong predictors for fetal lipids and fetal growth. Infants with abnormal growth seem to be exposed to a distinct intrauterine environment compared with those with appropriate growth.

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Section: Schaefer-graf and Associatessupporting

confidence: 90%

Maternal Lipids as Strong Determinants of Fetal Environment and Growth in Pregnancies With Gestational Diabetes Mellitus

Schaefer-Graf

K²,

Kulbacka³

et al. 2008

Diabetes Care

392

263

View full text Add to dashboard Cite

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“…Decreased body size could prompt an increase in ␤-cell mass, leading to increased insulin secretion in an attempt to normalize body size by promoting growth. A similar adaptive response may be seen in small-for-gestational-age humans, who manifest insulin levels 2.5-fold higher than controls (44), mirroring hyperinsulinemia in young FASDEL mice (Fig. 3A, bottom).…”

Section: Discussionsupporting

confidence: 65%

Decreased Fetal Size Is Associated With β-Cell Hyperfunction in Early Life and Failure With Age

et al. 2008

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OBJECTIVE— Low birth weight is associated with diabetes in adult life. Accelerated or “catch-up” postnatal growth in response to small birth size is thought to presage disease years later. Whether adult disease is caused by intrauterine β-cell–specific programming or by altered metabolism associated with catch-up growth is unknown. RESEARCH DESIGN AND METHODS— We generated a new model of intrauterine growth restriction due to fatty acid synthase (FAS) haploinsufficiency (FAS deletion [FASDEL]). Developmental programming of diabetes in these mice was assessed from in utero to 1 year of age. RESULTS— FASDEL mice did not manifest catch-up growth or insulin resistance. β-Cell mass and insulin secretion were strikingly increased in young FASDEL mice, but β-cell failure and diabetes occurred with age. FASDEL β-cells had altered proliferative and apoptotic responses to the common stress of a high-fat diet. This sequence appeared to be developmentally entrained because β-cell mass was increased in utero in FASDEL mice and in another model of intrauterine growth restriction caused by ectopic expression of uncoupling protein-1. Increasing intrauterine growth in FASDEL mice by supplementing caloric intake of pregnant dams normalized β-cell mass in utero. CONCLUSIONS— Decreased intrauterine body size, independent of postnatal growth and insulin resistance, appears to regulate β-cell mass, suggesting that developing body size might represent a physiological signal that is integrated through the pancreatic β-cell to establish a template for hyperfunction in early life and β-cell failure with age.

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“…Some authors have suggested that IR, as a consequence of intrauterine growth retardation would be detectable as early as birth (7,8). On the other hand, there is evidence that increased insulin sensitivity induced by the fetal environment aims at ameliorating nutrient disposal and utilization, ultimately leading to fetal growth (9). In this respect, an increase in insulin sensitivity would be a physiological adaptation to fetal growth restriction because insulin is a major regulator of fetal growth.…”

Section: Introductionmentioning

confidence: 99%

Retinol-binding protein 4 in neonates born small for gestational age

Giacomozzi

Ghirri

Lapolla

et al. 2010

J Endocrinol Invest

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ABSTRACT. Background: Retinol-binding protein 4 (RBP4) is an adipocyte-derived 'signal' that may contribute to the pathogenesis of insulin resistance and Type 2 diabetes. The relationship of RBP4 with insulin resistance and metabolic risk in human beings has been the subject of several studies. Subjects born small for gestational age (SGA) are at risk of insulin resistance and Type 2 diabetes. Though RBP4 could represent an early marker of insulin resistance, to date, none have determined RBP4 in SGA children. Aim: Our aim was to measure RBP4 concentrations in cord blood of SGA newborns compared with those in children born with a birth weight appropriate for gestational age (AGA) and to determine whether serum RBP4 levels at birth correlate with insulin sensitivity markers. Subjects and methods: Sixty-four newborns, 17 born SGA (mean gestational age: 36.4±2.1 weeks), and 47 born AGA (mean gestational age: 37.0±3.6 weeks) were studied. The main outcome measures included anthropometry, lipid profile, insulin, homeostasis model assessment, quantitative insulin-sensitivity check index, adiponectin, and RBP4. Results: RBP4 concentrations were significantly reduced in SGA newborns (p<0.002). No relationship was found between RBP4 and insulin sensitivity parameters. Stepwise regression analysis revealed that birth weight was the major predictor of RBP4 serum concentrations (p<0.001). Conclusion: RBP4 is reduced in SGA newborns, birth weight representing the major determinant of RBP4 concentrations, and is not related to insulin sensitivity. No significant difference in adiponectin levels and insulin sensitivity markers was found between SGA and AGA neonates. INTRODUCTIONRetinol-binding protein 4 (RBP4) is an adipocyte-derived 'signal' that may contribute to the pathogenesis of insulin resistance (IR) and Type 2 diabetes. RBP4 could play a role in obesity-induced IR, since chronic elevation of RBP4 in mice increases hepatic glucose production, down-regulates insulin signaling in muscle, and causes systemic IR (1). Furthermore, lowering elevated serum RBP4 levels in obese mice with a synthetic retinoid improves insulin sensitivity and normalizes glucose tolerance (1). In humans, the link between RBP4 and IR is less clear. In adulthood, serum RBP4 levels have been shown to correlate with the magnitude of IR in subjects with obesity, impaired glucose tolerance, and Type 2 diabetes (2). Moreover, elevated serum RBP4 was associated with components of the metabolic syndrome, including increased body mass index, waist-tohip ratio, serum triglyceride levels, and systolic blood pressure and decreased HDL cholesterol levels (2). In childhood, a relationship between serum RBP4 and obesity and components of the metabolic syndrome has been described in pre-pubertal and early pubertal children (3).Increased risk of developing IR and Type 2 diabetes in adulthood is associated with low birth weight (4). Although this association is clearly established in adults (5), results in children are still conflicting (6). Some authors have sugg...

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Glucose and Lipid Metabolism in Small-for-Gestational-Age Infants at 72 Hours of Age

Abstract: In this study, SGA neonates displayed profiles suggestive of lower insulin sensitivity and less favorable lipid metabolism in the early postnatal period.

Cited by 55 publications

References 28 publications

Maternal Lipids as Strong Determinants of Fetal Environment and Growth in Pregnancies With Gestational Diabetes Mellitus

Maternal Lipids as Strong Determinants of Fetal Environment and Growth in Pregnancies With Gestational Diabetes Mellitus

Decreased Fetal Size Is Associated With β-Cell Hyperfunction in Early Life and Failure With Age

Retinol-binding protein 4 in neonates born small for gestational age

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