Glucose and Lipid Metabolism in Small For Gestational Age Infants at 48 Hours of Age

Bazaes, Rodrigo; Salazar, Teresa; Pittaluga, E; Peña, Verónica; Alegria, Angelica; Íñiguez, Germán; Ong, Ken K.; Dunger, David B.; Mericq, Verónica

doi:10.1542/peds.111.4.804

Cited by 120 publications

(80 citation statements)

References 27 publications

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“…As previously reported for the complete cohort [11], at age 48 h the SGA infants had lower insulin levels (median 34.4 vs 59.7 pmol/l, p=0.03; Table 1) than the AGA infants. In contrast, at age 3 years, the SGA infants had higher fasting insulin levels (median 38.9 vs 23.8 pmol/l, p=0.005; Fig.…”

Section: Resultssupporting

confidence: 82%

“…We have previously reported that SGA infants have lower insulin levels at around the time of birth than AGA infants [11], but by the age of 1 year SGA infants, who showed catch-up weight gain (gain in weight SD score, >0.67), had higher fasting insulin levels and insulin resistance [9]. We now show that gains in weight SD score, or upward weight centile crossing, continued to the age of 3 years in SGA infants, and their insulin resistance also continued to progress during this period.…”

Section: Discussionmentioning

confidence: 94%

“…Weight was measured using a manual scale with a 10-g graduation (Seca, Quickmedical, Snoqualme, WA, USA). Forty-eight hours after birth, a pre-feeding 3-ml blood sample was obtained for determination of glucose, insulin and other markers of insulin sensitivity and secretion, as previously reported [11]. At 1 and 3 years of age, a short IVGTT was performed after an overnight fast (mean duration of fast, 9 h).…”

Section: Measurementsmentioning

confidence: 99%

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Longitudinal changes in insulin sensitivity and secretion from birth to age three years in small- and appropriate-for-gestational-age children

et al. 2005

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Aims/hypothesis: Insulin resistance and type 2 diabetes risk in human subjects who were small-for-gestationalage (SGA) at birth may be a consequence of rapid early postnatal weight gain. Materials and methods: We prospectively studied early changes in fasting insulin sensitivity and insulin secretion, assessed by a short intravenous glucose tolerance test that was conducted several times from birth to 3 years of age in 55 SGA (birthweight below fifth percentile) newborns and in 13 newborns with a birthweight appropriate for gestational age (AGA). Results: Most SGA infants showed postnatal upward weight centile crossing and by 3 years were similar in size to AGA infants. SGA infants had lower pre-feed insulin levels at postnatal age 48 h than AGA infants (median 34.4 vs 59.7 pmol/l, p<0.05), but by the age of 3 years they had higher fasting insulin levels (median 38.9 vs 23.8 pmol/l, p<0.005), which were related to rate of weight gain between 0 and 3 years (r=0.47, p=0.0003). First-phase insulin secretion did not differ between SGA and AGA infants, but SGA infants had a lower glucose disposition index (beta cell compensation) (median 235 vs 501 min mmol, p=0.02), which persisted after allowing for postnatal weight gain (p=0.009). Conclusions/interpretation: SGA infants showed a marked transition from lower pre-feed insulin and increased insulin sensitivity at birth to insulin resistance over the first 3 years of life. This transition was related to rapid postnatal weight gain, which could indicate a propensity to central fat deposition. The additional observation of reduced compensatory beta cell secretion underlines the need for long-term surveillance of glucose homeostasis in all SGA subjects, whether or not they show postnatal catch-up growth.

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Section: Resultssupporting

confidence: 82%

Section: Discussionmentioning

confidence: 94%

Section: Measurementsmentioning

confidence: 99%

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Longitudinal changes in insulin sensitivity and secretion from birth to age three years in small- and appropriate-for-gestational-age children

et al. 2005

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“…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. Consistent with this, we and others have reported that smallfor-gestational age (SGA) newborns display increased insulin sensitivity (10)(11)(12). Although RBP4 may play a pivotal role in the development of IR in humans, to date, however, no study has been carried out in low birth weight subjects.…”

Section: Introductionsupporting

confidence: 74%

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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“…Postnatal catch-up weight gain indicates a reversal from intra-uterine growth restraint [22,23] and observational data suggest that it could be mediated by increased postnatal appetite [24,25]. Alternatively, case control studies [26] and animal models of severe fetal growth restraint [1] suggest that insulin sensitivity and tissue insulin receptor number may paradoxically be initially increased, and this could also contribute to more rapid early weight gain. Whatever the explanation, early postnatal catch-up weight gain, or upward weight centile crossing in the first years of life, seems to predict the development of childhood obesity [5,6,7] and insulin resistance, and seems to underlie the association between reduced insulin sensitivity and smaller size at birth in our study.…”

Section: Discussionmentioning

confidence: 99%

Insulin sensitivity and secretion in normal children related to size at birth, postnatal growth, and plasma insulin-like growth factor-I levels

et al. 2004

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Aims/hypothesis. Type 2 diabetes risk is associated with low birth weight, rapid weight gain during childhood, and shorter stature and lower circulating IGF-I levels in adults. The largest variations in growth rates occur during the first postnatal years. We hypothesised that early postnatal variations in height and weight gain and IGF-I levels may be associated with risk markers for adult disease. Methods. We measured the fasting insulin sensitivity (Homeostasis model) and insulin secretion post-oral glucose (insulinogenic index 0-30 min) in 851 normal 8-year-old children from a prospective birth cohort. We examined associations between size at birth, postnatal weight gain and circulating IGF-I levels with insulin sensitivity and secretion at 8 years of age. Results. Fasting insulin sensitivity at 8 years was closely related to current BMI (r=−0.33, p<0.0005). Lower insulin sensitivity and higher BMI and waist circumference were all predicted by greater weight gain between birth to 3 years of age (all p<0.0005); lower birth weight was associated with reduced insulin sensitivity only in the highest current BMI tertile (r=0.17, p=0.006). In contrast, lower insulin secretion was related to smaller size at birth (p=0.01), independent of postnatal weight gain and insulin sensitivity. Lower insulin secretion was also independently related to shorter stature at 8 years of age relative to parental height (p=0.047) and with lower plasma IGF-I levels at 5 years of age (n=252, p=0.004). Conclusions/interpretation. Associations between lower birth weight and insulin resistance may be dependent on rapid weight gain during the early postnatal years. However, irrespective of postnatal weight gain, smaller size at birth, lower IGF-I levels and lower childhood height predicted reduced compensatory insulin secretion.

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Glucose and Lipid Metabolism in Small For Gestational Age Infants at 48 Hours of Age

Cited by 120 publications

References 27 publications

Longitudinal changes in insulin sensitivity and secretion from birth to age three years in small- and appropriate-for-gestational-age children

Longitudinal changes in insulin sensitivity and secretion from birth to age three years in small- and appropriate-for-gestational-age children

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

Insulin sensitivity and secretion in normal children related to size at birth, postnatal growth, and plasma insulin-like growth factor-I levels

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