Increased adrenocortical and adrenomedullary hormonal activity in 12-year-old children born small for gestational age

Tenhola, Sirpa; Martikainen, Anneli; Rahiala, Eero; Parviainen, Markku; Halonen, Pirjo; Voutilainen, Raimo

doi:10.1067/mpd.2002.126923

Cited by 54 publications

(44 citation statements)

References 21 publications

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“…Our present F levels were about 23% lower than those measured by an EIA assay (21), which is most probably due to the lack of interferences and cross-reactions often detected in immunoassays. Our F/E ratios were also somewhat lower than those derived from immunologic assays by Dötsch and coworkers (22).…”

Section: Discussionmentioning

confidence: 51%

“…The detection limit of the assay was 2 nmol/L of F and 3 nmol/L of E based on a signal-to-noise ratio of 3. F concentrations from the same serum samples had been analysed previously by DPC Immulite 2000, chemiluminescent enzyme immunoassay, EIA (Diagnostic Products Corporation, Los Angeles, CA) (21). The EIA-measured F concentrations correlated well with the LC-MS/MS-measured ones in both the SGA and AGA groups (r ϭ 0.934, p Ͻ 0.001; r ϭ 0.904, p Ͻ 0.001, respectively).…”

Section: Serum F and E Lc-ms/ms Assaysmentioning

confidence: 56%

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Association of Serum Lipid Concentrations, Insulin Resistance Index and Catch-Up Growth with Serum Cortisol/Cortisone Ratio by Liquid Chromatography Tandem Mass Spectrometry in Children Born Small for Gestational Age

et al. 2005

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Section: Discussionmentioning

confidence: 51%

Section: Serum F and E Lc-ms/ms Assaysmentioning

confidence: 56%

Association of Serum Lipid Concentrations, Insulin Resistance Index and Catch-Up Growth with Serum Cortisol/Cortisone Ratio by Liquid Chromatography Tandem Mass Spectrometry in Children Born Small for Gestational Age

et al. 2005

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“…This lower BMI may explain the lower basal 11␤-HSD-1 activity, but not the higher GC-stimulated activity. Enhanced generation of cortisol from cortisone after GC stimulation may explain the enhanced reactivity to stress in SGA individuals and may contribute to their metabolic morbidity in adult life (20,55). We found GC-stimulated 11␤-HSD-1 activity to correlate inversely with birth weight (the degree of SGA) and GA (prematurity).…”

Section: Discussionmentioning

confidence: 61%

11β–Hydroxysteroid Dehydrogenase Type 1 Activity in Short Small-For-GA Children and in Response to GH Therapy

et al. 2011

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Small for GA (SGA) children are at risk for developing the metabolic syndrome. Those who do not catch up, and remain short (SSGA), may benefit from GH therapy. 11␤ Hydroxysteroid dehydrogenase type 1 (11␤-HSD-1) is expressed in visceral fat and is implicated in metabolic morbidity. We hypothesized that SSGA children will have increased basal and glucocorticoid (GC)-stimulated 11␤-HSD-1 activity. Twenty SSGA children, aged 7.1 Ϯ 1 y (mean Ϯ SD), were studied before and while on GH therapy and compared with 12 normal age-matched controls. 11␤-HSD-1 activity was evaluated by gas chromatography mass spectrometry (GCMS) of urinary steroid product/substrate ratios. GC-stimulated 11␤-HSD-1 activity was assessed after overnight dexamethazone (DEX), by oral cortisone conversion to cortisol. In SSGA children, 11␤-HSD-1 activity was lower (p Ͻ 0.05) and GC-stimulated activity enhanced. SSGA children had maximal cortisol generation of 883 Ϯ 108 compared with 690 Ϯ 63 nmol/L in controls (p Ͻ 0.04). GH treatment suppressed 11␤-HSD-1 activity. GC-stimulated enzyme activity correlated negatively with GA (r ϭ Ϫ0.53, p Ͻ 0.01) and birth weight (r ϭ Ϫ0.55, p Ͻ 0.01). SSGA is associated with enhanced GC-stimulated 11␤-HSD-1 activity. This may be programmed in utero, as it is not a function of body composition or secondary metabolic derangement. GH therapy normalizes GCstimulated 11␤-HSD-1 activity. (Pediatr Res 70: 208-212, 2011) B y definition, 5-10% of all neonates are born small for GA (SGA). Some of these children do not catch up (1,2) and remain short. They may benefit from GH therapy (3-5). This subgroup is designated in this article as short SGA (SSGA). Regardless of their later growth pattern, SGA children are at risk for developing the metabolic syndrome later in life (6 -10). This increased risk for future morbidity has been documented more in SGA individuals who had catch up growth (11-13), than in those who did not (14 -16).Fetal programming might be coupled with several endocrine pathways (17), including the hypothalamic-pituitaryadrenal (HPA) axis (18 -20). Indeed, elevated cortisol levels have been reported for adults born SGA (21) and in SSGA children (22)(23)(24). Elevated cortisol levels may also be involved in pre-and postnatal growth, as demonstrated by the inverse correlation between cortisol levels in cord blood and embryo length gained during the first trimester in intrauterine growth retarded (IUGR) children (25) .Prereceptor modulation of cortisol by 11␤-hydroxysteroid dehydrogenase type 1 (11␤-HSD-1) converts cortisone to cortisol for intracrine action (26). Among other regulatory mechanisms of enzyme activity (27), GH inhibits 11␤-HSD-1 activity and gene expression, while GH deficiency is associated with enhanced enzyme activity (28 -31).The working hypotheses of this study were that SSGA children will have increased basal and GC-stimulated 11␤-HSD-1 activity and that these will be inhibited by GH treatment. Toward these hypotheses, we studied in vivo 11␤-HSD-1 activity, as measured by the ratio...

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“…The means of adiponectin, cortisol, FCI, or GBA did not differ between the SGA subgroups with good and poor catch-up growth (detailed data not shown). It is worth noting that the SGA subjects were shorter, lighter, and slimmer (in terms of weight for height, body mass index (BMI), waist circumference (WC), and WC/height ratio) than the AGA controls (Table 1), but their pubertal development stage did not differ from that of the controls at the time of evaluation (14).…”

Section: Resultsmentioning

confidence: 99%

“…In children, Clark et al reported an association between low birth weight and increased urinary glucocorticoid metabolite excretion (11), while other investigators have not been able to show any association between birth size and circulating cortisol concentrations (12)(13)(14)(15)(16). Thus, according to these studies, the association between fetal growth restriction and later increased glucocorticoid activity in humans is still controversial, at least during childhood.…”

Section: Introductionmentioning

confidence: 99%

Serum glucocorticoids and adiponectin associate with insulin resistance in children born small for gestational age

Tenhola¹,

Todorova²,

Jääskeläinen³

et al. 2010

European Journal of Endocrinology

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Objectives: Altered glucocorticoid activity is one possible mechanism linking fetal growth restriction with later insulin resistance (IR) and type 2 diabetes. We aimed to investigate whether serum glucocorticoid parameters are related to IR in children born small for gestational age (SGA). Design: A total of 110 children (55 age-and gender-matched pairs born SGA or appropriate for gestational age (AGA) in a case-control setting) were studied at the mean age of 12.2 (S.D. 0.2) years. Methods: Serum cortisol, corticosteroid-binding globulin (CBG), free cortisol index (FCIZcortisol/CBG), and glucocorticoid bioactivity (GBA, transactivation assay) were analyzed and related to serum adiponectin and insulin-like growth factor-binding protein 1 (IGFBP1) concentrations and homeostasis model assessment for IR (HOMA-IR) and QUICKI indices. Results: In the pooled study population, GBA correlated well with cortisol and FCI (rZ0.681 and 0.586 respectively; P!0.001 for both). Serum cortisol, CBG, FCI, GBA, HOMA-IR, or QUICKI did not differ between the SGA and AGA subjects, but the SGA children had lower body mass index (PZ0.005) and waist circumference (WC) (PZ0.001). The mean GBA in the highest GBA quartile was higher among the SGA subjects than among the AGA subjects (138.6 vs 96.4 nmol/l cortisol equivalents, P!0.001). In the SGA children, GBA correlated positively with HOMA-IR (rZ0.522, P!0.001) and inversely with adiponectin (rZK0.278, PZ0.042) (WC/height ratio adjustments), and in logistic regression analysis, higher GBA (odds ratio (OR) 1.3; PZ0.013), lower adiponectin (OR 1.4; PZ0.038), and lower IGFBP1 (OR 1.9; PZ0.010) associated independently with higher HOMA-IR. Conclusions: These findings suggest that increased glucocorticoid activity and low serum adiponectin concentrations associate with IR in SGA children.

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Increased adrenocortical and adrenomedullary hormonal activity in 12-year-old children born small for gestational age

Cited by 54 publications

References 21 publications

Association of Serum Lipid Concentrations, Insulin Resistance Index and Catch-Up Growth with Serum Cortisol/Cortisone Ratio by Liquid Chromatography Tandem Mass Spectrometry in Children Born Small for Gestational Age

Association of Serum Lipid Concentrations, Insulin Resistance Index and Catch-Up Growth with Serum Cortisol/Cortisone Ratio by Liquid Chromatography Tandem Mass Spectrometry in Children Born Small for Gestational Age

11β–Hydroxysteroid Dehydrogenase Type 1 Activity in Short Small-For-GA Children and in Response to GH Therapy

Serum glucocorticoids and adiponectin associate with insulin resistance in children born small for gestational age

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