Metabolic consequences of intrauterine growth retardation

Gluckman, P. D.; Cutfield, Wayne S.; Harding, JE; Milner, Danny A.; Jensen, Ellen C.; Woodhall, S; Gallaher, B. W.; Bauer, MK; Breier, B. H.

doi:10.1111/j.1651-2227.1996.tb14282.x

Cited by 45 publications

(26 citation statements)

References 26 publications

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“…High insulin levels could, later in life, stimulate early secretion of luteinizing hormone, leading to early puberty (2,28,29). Nevertheless, in most of the children born SGA in our sample, the course and timing of puberty were within the normal range.…”

Section: Discussionmentioning

confidence: 83%

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Pubertal course of persistently short children born small for gestational age (SGA) compared with idiopathic short children born appropriate for gestational age (AGA)

Lazar¹,

Pollak²,

Kalter‐Leibovici³

et al. 2003

Eur J Endocrinol

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Objective: Few data are available on the pubertal development of children born small for gestational age (SGA) who fail to show catch-up growth. Design: A longitudinal analysis compared the pubertal course of persistently short children born SGA compared to children with idiopathic short stature who were appropriate for gestational age (AGA). One hundred and twenty-eight short children (height SDS , 21.7), including 76 (31 boys) born SGA and 52 (22 boys) born AGA, were regularly followed from early childhood to completion of puberty. Results: Puberty was attained at normal age (10.5 -14 years in boys, 9.5-13 years in girls) for most children in both the SGA and AGA groups (boys, 80% and 77%; girls, 76% and 78% respectively). The duration of puberty was similar in the SGA and AGA groups. Menarche occurred at normal age range but was significantly earlier in the SGA girls (P , 0.01 by ANOVA). Despite the similar total pubertal growth, the patterns of growth differed significantly: SGA group -accelerated growth and bone maturation rates from onset of puberty with peak height velocity at Tanner stages 2-3, followed by a decelerated growth rate and earlier fusion of the epiphyses; AGA group -steady progression of bone elongation and maturation throughout puberty (pubertal growth, P , 0.05 in both sexes; bone maturation, P , 0.001 in both sexes). Final height in the SGA group was compromised compared with their target height (P , 0.001). Conclusion: Children born SGA have a normal pubertal course with a distinct pubertal growth pattern. This pattern may represent an altered regulation of their growth modalities.

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Section: Discussionmentioning

confidence: 83%

“…These are also maintained postnatally (1,2) and may affect the long-term pattern of postnatal growth and development. A number of longitudinal studies have shown that although the majority of children born small for gestational age (SGA) exhibit significant catch-up growth during the first 6-12 months of life, about 10 -17% do not.…”

Section: Introductionmentioning

confidence: 99%

Pubertal course of persistently short children born small for gestational age (SGA) compared with idiopathic short children born appropriate for gestational age (AGA)

Lazar¹,

Pollak²,

Kalter‐Leibovici³

et al. 2003

Eur J Endocrinol

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“…Programming of the endocrine mechanisms of foetal growth which are mediated by insulin and insulin like growth factors (IGF) have been implicated. 20 In our sample population, we have previously reported an Abdominal fat and birth size in children SP Garnett et al inverse relation between IGF-I concentrations at age 7=8 y and birth size -children with the lowest birth size and heaviest current weight had the highest IGF-I concentrations. 21 High concentrations may reflect persisting IGF-I resistance or alternatively be a response to adequate postnatal nutrition and hence be a feature of rapid postnatal growth.…”

Section: Discussionmentioning

confidence: 96%

Abdominal fat and birth size in healthy prepubertal children

et al. 2001

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BACKGROUND: Studies examining the foetal origins hypothesis suggest that small birth size may be a marker of foetal adaptations that programme future propensity to adult disease. We explore the hypothesis that birth size may relate to fat distribution in childhood and that fat distribution may be a link between birth size and adult disease. OBJECTIVE: To investigate the relationship between birth size and abdominal fat, blood pressure, lipids, insulin and insulin:glucose ratio in prepubertal children. DESIGN: Cross-sectional study, based on a birth cohort of consecutive full-term births. SUBJECTS: Two hundred and fifty-five (137 females) healthy, 7-and 8-y-old children. MEASUREMENTS: Body composition and abdominal fat was measured by dual energy X-ray absorptiometry. Lipid, glucose and insulin profiles were measured after an overnight fast and an automated BP monitor was used for blood pressure measurements. RESULTS: There was a negative association between abdominal fat and birth weight s.d. score across a range of normal birth weights (b ¼ 70.18; 95% CI ¼ 70.31 to 70.04, P ¼ 0.009) and a positive association with weight s.d. score at 7=8 y (b ¼ 0.35; 95% CI ¼ 0.24 to 0.46, P < 0.001). Children who were born with the lowest weight s.d. score and had the greatest weight s.d. score at 7=8 y had significantly more (P < 0.001) abdominal fat, as a percentage of total fat (6.53 AE 1.3%) than those who had the highest birth weight s.d. score and the lowest weight s.d. score at 7=8 y (4.14 AE 0.5%). Similar results were seen if head circumference, but not ponderal index, was used as an indicator of birth size. Increased abdominal fat was associated with higher total cholesterol:HDL cholesterol, higher triglyceride concentration and increased diastolic blood pressure. CONCLUSIONS: Birth weight independently predicted abdominal fat. Children with the highest amount of abdominal fat were those who tended to be born lighter and gained weight centiles. Increased abdominal fat was associated with precursor risk factors for ischaemic heart disease.

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“…This system consisted of a To verify the specificity of the changes in the PeN, the number of grains in SS mRNA-expressing neurons in the cortex of adult rats was also analyzed. From each animal, a total of 100 cortical cells, divided over five to eight slides, were analyzed at the level of bregma Ϫ0.26 mm to Ϫ1.80 mm (14). Cells were considered labeled when the number of silver grains overlying the cytoplasm were greater than 10 times the background levels.…”

Section: Methodsmentioning

confidence: 99%

Effects of Intrauterine and Early Postnatal Growth Restriction on Hypothalamic Somatostatin Gene Expression in the Rat

et al. 2000

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Metabolic consequences of intrauterine growth retardation

Abstract: This review focuses on intrauterine growth retardation (IUGR) occurring spontaneously and without a defined infective, toxic or genetic cause. Such fetal growth retardation is generally thought to be a consequence of inadequate provision of nutritional substrates across the placenta.

Cited by 45 publications

References 26 publications

Pubertal course of persistently short children born small for gestational age (SGA) compared with idiopathic short children born appropriate for gestational age (AGA)

Pubertal course of persistently short children born small for gestational age (SGA) compared with idiopathic short children born appropriate for gestational age (AGA)

Abdominal fat and birth size in healthy prepubertal children

Effects of Intrauterine and Early Postnatal Growth Restriction on Hypothalamic Somatostatin Gene Expression in the Rat

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