| 1. |
- Ahlsson, Fredrik, et al.
(author)
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Insulin Resistance, a Link between Maternal Overweight and Fetal Macrosomia in Nondiabetic Pregnancies
- 2010
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In: Hormone research in paediatrics. - : S. Karger AG. - 1663-2818 .- 1663-2826. ; 74:4, s. 267-274
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Journal article (peer-reviewed)abstract
- Background/Aims: During the last decades the number of large for gestational age infants delivered by nondiabetic mothers has increased. Our aim was to investigate to what extent fetal growth in nondiabetic pregnant women can be explained by rates of maternal energy substrate production and resting energy expenditure. Methods: Twenty nonsmoking pregnant women without impaired glucose tolerance and with a wide range of fetal weights (0.2-2.7 SDS) were investigated at 36 weeks of gestation. Maternal lipolysis, glucose production, resting energy expenditure, body composition and insulin resistance were assessed.Results: Median (range) glucose production rate was 805 (653-1,337) mumol/min and that of glycerol, reflecting lipolysis, was 214 (110-576) mumol/min. Multiple linear regression analysis showed that maternal fat mass explained 36% of the variation in insulin resistance, accounting for 62% of the variation in glucose production. Further, glucose production explained 31% of the variation in fetal weight. Resting energy expenditure explained 51% of the variation in estimated fetal weight. Conclusion: Fetal weight is dependent on maternal glucose production, which is in turn determined by the degree of insulin resistance, induced in part by the maternal fat mass. The variation in maternal resting energy expenditure is closely related to fetal weight.
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| 2. |
- Ahmed, SF, et al.
(author)
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Promoting growth in chronic inflammatory disease: lessons from studies of the growth plate
- 2009
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In: Hormone research. - : S. Karger AG. - 1423-0046. ; 7272 Suppl 1, s. 42-47
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Journal article (peer-reviewed)abstract
- <i>Background:</i> Growth disorders are commonly observed in children with chronic inflammatory disease. It is likely that these disorders are mediated by a combination of factors, including the disease process and its treatment (with drugs such as glucocorticoids [GCs]). These factors affect the growth hormone-insulin-like growth factor I (IGF-I) axis, which is crucial for promoting linear growth at the level of the growth plate. Recent advances in our knowledge of the effects of GCs and proinflammatory cytokines on the growth plate have led to an improved understanding of the biological rationale for the use of growth-promoting therapy in children with chronic inflammatory disease and concurrent growth retardation. <i>Conclusions:</i> Both GCs and proinflammatory cytokines can adversely affect a number of components of growth plate chondrogenesis, and these effects can be ameliorated by raising local IGF-I exposure. However, this intervention does not lead to complete normalization of the growth plate. In children with chronic inflammation, the cornerstone of improving growth remains the judicious use of GCs while ensuring effective control of the disease process.
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| 3. |
- Akram, SK, et al.
(author)
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Placental IGF-I, estrogen receptor, and progesterone receptor expression, and maternal anthropometry in growth-restricted pregnancies in the Swedish population
- 2011
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In: Hormone research in paediatrics. - : S. Karger AG. - 1663-2826 .- 1663-2818. ; 75:2, s. 131-137
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Journal article (peer-reviewed)abstract
- <i>Background/Aims:</i> Fetal growth restriction is a complex problem of pregnancy arising from multiple etiologies. Key regulatory elements of growth are the insulin-like growth factor (IGF) axis, and estrogen and progesterone receptors. The aims were to determine the relations of expression of IGF-I, estrogen receptors α and β (ERα and ERβ, respectively), and progesterone receptor (PR), with maternal anthropometry, focusing on birth weight outcomes. <i>Methods:</i> Placental samples were obtained from 33 patients following delivery. mRNA expression was determined by a solution hybridization technique. Samples were divided into normal control (NC) and growth-restricted (GR) groups. <i>Results:</i> IGF-I expression was lower in the GR as compared to the NC group. PR levels correlated positively with IGF-I expression, infant anthropometry, and gestational age (GR). ERα correlated positively with PR expression (NC), and maternal BMI at delivery (GR). ERβ correlated positively with maternal delivery weight and gestational age (NC). <i>Conclusion:</i> The differences in placental expression of IGF-I emphasize its key role in birth weight outcomes. We further suggest the importance of PR expression in the pathogenesis of intrauterine growth restriction, as there were direct correlations of PR expression with both IGF-I expression and infant anthropometric parameters, as well as gestational age.
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| 4. |
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| 5. |
- Albertsson-Wikland, Kerstin, 1947, et al.
(author)
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Growth hormone dose-dependent pubertal growth : a randomized trial in short children with low growth hormone secretion
- 2014
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In: Hormone Research in Paediatrics. - : S. Karger AG. - 1663-2818 .- 1663-2826. ; 82:3, s. 158-170
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Journal article (peer-reviewed)abstract
- Background/Aims: Growth hormone (GH) treatment regimens do not account for the pubertal increase in endogenous GH secretion. This study assessed whether increasing the GH dose and/or frequency of administration improves pubertal height gain and adult height (AH) in children with low GH secretion during stimulation tests, i. e. idiopathic isolated GH deficiency.Methods: A multicenter, randomized, clinical trial (No. 88-177) followed 111 children (96 boys) at study start from onset of puberty to AH who had received GH(33) mu g/kg/day for >= 1 year. They were randomized to receive 67 mu g/kg/day (GH(67)) given as one (GH(67x1); n = 35) or two daily injections (GH(33x2); n = 36), or to remain on a single 33 mu g/kg/day dose (GH(33x1); n = 40). Growth was assessed as height SDS gain for prepubertal, pubertal and total periods, as well as AH SDS versus the population and the midparental height.Results: Pubertal height SDS gain was greater for patients receiving a high dose (GH(67), 0.73) than a low dose (GH(33x1), 0.41, p < 0.05). AH(SDS) was greater on GH(67) (GH(67x1), -0.84; GH(33x2), -0.83) than GH(33) (-1.25, p < 0.05), and height SDS gain was greater on GH(67) than GH(33) (2.04 and 1.56, respectively; p < 0.01). All groups reached their target height SDS.Conclusion: Pubertal height SDS gain and AH SDS were dose dependent, with greater growth being observed for the GH(67) than the GH(33) randomization group; however, there were no differences between the once-and twice-daily GH(67) regimens. (C) 2014 S. Karger AG, Basel.
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| 6. |
- Albertsson-Wikland, Kerstin, 1947, et al.
(author)
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New Reference for Height in Swedish Boys and Girls
- 2014
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In: Hormone Research in Paediatrics. 82 (suppl 1), s. 256. 53rd Annual Meeting of the European Society for Paediatric Endocrinology (ESPE). Dublin, Ireland, September 18-20, 2014. Hormone Research in Paediatrics.. - : S. Karger AG. - 1663-2818 .- 1663-2826.
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Conference paper (other academic/artistic)abstract
- Background: The actual Swedish growth references are based on a cohort born 1974. Objective and hypotheses: Due to secular changes there is need for new height references. Method: Material: Height measurements from birth to adult height (AH) in a cohort of healthy, Nordic and born full term 1990, 20.796 from 1647 boys, 19.202 from 1501 girls were used (ALL) and compared to both a subgroup with puberty close to mean (PHV G0.25 years) of 3.726 heights from 259 boys; 3.759 from 271 girls, and a subgroup (AM) with O10 height measurements evenly distributed (15.324 in 989 boys; 14.381 in 919 girls), and of high data quality. The 1974 cohort, with similar subgrouping, were used for comparison. Methods: For construction of height curves the LMS method was applied with LMS parameters based directly on the data: the power in the Box-Cox transformation (L), the median (M), and the generalized coefficient of variation (S). The GAMLSS R-package with a special LMS program was used, giving L, M, S and optional kurtosis as functions of age. Results: Height reference curves, with mean, G1, G2 SDS were obtained for 1990 of the ALL vs the AM material with similar results whereas the close puberty material showed the same mean but more narrow G1, G2 SDS during adolescence. When the different 1990 references were compared to 1974 references, the corresponding 1974 differences were found. The new references takes into account that the 1990 cohort had a more rapid infancy growth, increased prepubertal growth, especially in boys, increased pubertal gain, only in girls, and increased AH in both genders.
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| 7. |
- Albin, Anna-Karin, et al.
(author)
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Does growth hormone treatment influence pubertal development in short children?
- 2011
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In: Hormone Research in Paediatrics. - : S. Karger AG. - 1663-2826 .- 1663-2818. ; 76:4, s. 262-72
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Journal article (peer-reviewed)abstract
- AIM: To study the influence of growth hormone (GH) treatment on the initiation and progression of puberty in short children. METHODS: This prospective, randomized, controlled study included 124 short children (33 girls) who received GH treatment (Genotropin(R); Pfizer Inc.) from a mean age of 11 years until near adult height [intent-to-treat (ITT) population]. Children were randomized into three groups: controls (n = 33), GH 33 mug/kg/day (n = 34) or GH 67 mug/kg/day (n = 57). Prepubertal children at study start constituted the per-protocol (PP) population (n = 101). Auxological measurements were made and puberty was staged every 3 months. Serum sex-steroid concentrations were assessed every 6 months. RESULTS: No significant differences were found between the groups, of both PP and ITT populations, in time elapsed from start of treatment until either onset of puberty, age at start of puberty or age at final pubertal maturation in either sex. In the ITT population, pubertal duration was significantly longer in GH-treated girls, and maximum mean testicular volume was significantly greater in GH-treated boys than controls, but there were no differences in testosterone levels between the groups. CONCLUSION: GH treatment did not influence age at onset of puberty and did not accelerate pubertal development. In boys, GH treatment appeared to increase testicular volume.
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| 8. |
- Albin, Anna-Karin, et al.
(author)
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Estradiol and Pubertal Growth in Girls.
- 2012
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In: Hormone research in paediatrics. - : S. Karger AG. - 1663-2826 .- 1663-2818. ; 78:4
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Journal article (peer-reviewed)abstract
- Aim: The objective of this study was to determine estradiol levels and assess their relationship to pubertal growth in girls. Methods: Thirty-seven 24-hour profiles of serum 17β-estradiol were retrospectively analyzed in relation to growth in 27 healthy girls admitted for short/tall stature (n = 20) or recruited as healthy volunteers at Göteborg Pediatric Growth Research Center (GP-GRC). Inclusion Criteria: Birth weight and length above -2 SDS, gestational age 37-42 weeks, prepubertal height and weight within ±3 SDS and normal growth hormone secretion. Serum estradiol was determined by a validated ultrasensitive extraction radioimmunoassay (detection limit 4 pmol/l). A sixth-grade polynomial was fitted to each girl's growth data. Growth velocity and age at peak height velocity (PHV) was calculated. Results: A dose-response model was used to find the morning 17β-estradiol level at which half of the maximal pubertal growth up to PHV had occurred, EC(50), which was 20 pmol/l with a 95% confidence interval of 13-31. When 17β-estradiol exceeds early pubertal levels (Tanner breast stage 2, 10-51 pmol/l), less than 25% of the potential pubertal growth velocity up to PHV remains. Conclusions: Morning 17β-estradiol in the low early pubertal range (13-31 pmol/l) is associated with increasing growth velocity.
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| 9. |
- Albin, Anna-Karin, et al.
(author)
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Pubertal growth and serum testosterone and estradiol levels in boys.
- 2013
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In: Hormone research in pædiatrics. - : S. Karger AG. - 1663-2826 .- 1663-2818. ; 80:2, s. 100-10
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Journal article (peer-reviewed)abstract
- Background/Aims: To study serum testosterone and estradiol in healthy boys in relation to growth during puberty up to peak height velocity (PHV). Methods: Growth velocity was analyzed through testosterone (n = 41) and 17β-estradiol (n = 37) 24-hour profiles in a dose-response model. Participants were 26 healthy boys admitted for short or tall stature or participating as healthy volunteers at the Queen Silvia Children's Hospital. Other inclusion criteria included the following: gestational age 37-42 weeks, birth weight and length >-2 standard deviation score (SDS) and prepubertal height and weight within ±3 SDS. Testosterone was measured using a modified radioimmunoassay (RIA) with a detection limit of 0.03 nmol/l. Estradiol was determined using an ultrasensitive extraction RIA with a detection limit 4 pmol/l. A sixth-grade polynomial was fitted to each child's growth data, giving growth velocity and age at PHV. Results: Growth velocity increased by 50% from prepubertal growth to PHV at a morning testosterone level of 3.1 nmol/l (95% confidence interval 2.4-4.2), EC50. The corresponding EC50 of 17β-estradiol was 6.5 pmol/l (3.2-13). Boys approaching PHV (<4% remaining) had morning testosterone levels >10 nmol/l and 17β-estradiol >9 pmol/l. Conclusion: Observed early puberty/initial mid puberty morning testosterone levels of 2.4-4.2 nmol/l are associated with a 50% increase in growth velocity from prepubertal growth to PHV in healthy boys.
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| 10. |
- Allbrand, Marianne, 1958-, et al.
(author)
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Adipocytokines in placenta and cord blood in relation to maternal obesity, and foetal and postnatal growth of the child
- 2015
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In: Hormone Research in Paediatrics. - Basel, Switzerland : S. Karger. - 1663-2818 .- 1663-2826. ; 82:Suppl. 1, s. 47-48
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Journal article (other academic/artistic)abstract
- Background: The nutritional and hormonal state in utero may be a link between maternal obesity and obesity in the offspring. The gene expression in placentae in pregnancies complicated by diabetes is reduced for leptin, but increased for ghrelin. It is not known whether these genes’ expressions in placentae are altered in maternal obesity.Objectives and hypotheses: To compare obese and normal-weight women and their children concerning gene expressions of leptin and ghrelin in placentae; leptin, ghrelin, adiponectin, and C-peptide levels in cord blood, birth size and postnatal growth. Changes in the expression of these adipocytokines may lead to an altered hypothalamic sensitivity to leptin and ghrelin resulting in an increased risk of obesity in the offspring.Method: 32 women with pre-pregnancy obesity, but otherwise healthy, were compared to 32 matched, normal-weight controls. Full-term placenta biopsies were analysed with qPCR for leptin mRNA and ghrelin mRNA. Cord blood samples were examined with ELISA for leptin, ghrelin, adiponectin, and C-peptide concentrations. Birth size and postnatal growth of the children were collected from clinical registers at the Child Health Care Units.Results: The leptin and ghrelin gene expressions in placentae did not differ between obese and normal-weight women. The leptin concentration in cord blood was higher in children of obese mothers (P=0.021). It correlated with birth weight Z-score (r=0.467, P<0.001) and C-peptide level in cord blood (r=0.446, P<0.001). Children of obese women were slightly heavier at birth, but postnatal growth did not differ between groups. Children with birth weight ≤−0.67 Z-score had higher ghrelin levels in cord blood than heavier children (P=0.042). The leptin level in cord blood correlated negatively with weight gain at 6 months (r=−0.332, P=0.009). The ghrelin level in cord blood correlated with weight gain at 3 months in girls (r=0.611, P=0.001), but not in boys. The adiponectin level in cord blood correlated negatively with length gain at 3 years in the obese group (r=−0.571, P=0.033), but not in the normal-weight group.Conclusion: Leptin and ghrelin placental gene expressions are not altered in obese women, but foetal adipocytokine production may influence early postnatal growth, possibly by influencing hunger signalling or insulin levels
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