| 1. |
- 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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| 2. |
- Andersson, Björn, 1977, et al.
(author)
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Decrease in adiponectin levels correlates to growth response in growth hormone-treated children.
- 2009
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In: Hormone research. - : S. Karger AG. - 1423-0046 .- 0301-0163. ; 71:4, s. 213-8
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Journal article (peer-reviewed)abstract
- Adiponectin is secreted by adipose tissue and circulates in human plasma at high levels. Decreased adiponectin levels are associated with insulin resistance and obesity. The aim of this study was to investigate whether changes in serum adiponectin levels are related to the growth response, insulin levels and insulin resistance during growth hormone (GH) treatment.
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| 3. |
- Boguszewski, M. C., et al.
(author)
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Insulin-like growth factor-1, leptin, body composition, and clinical status interactions in children with cystic fibrosis
- 2007
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In: Horm Res. - : S. Karger AG. - 0301-0163. ; 67:5, s. 250-6
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Journal article (peer-reviewed)abstract
- BACKGROUND/AIMS: Children with cystic fibrosis (CF) are of increased risk of reduced fat body mass (FBM) and lean body mass (LBM). Serum concentrations of insulin-like growth factor-1 (IGF-1)and leptin could be markers of LBM and/or FBM depletion. To evaluate the relationships between disease activity, body composition, IGF-1 and leptin concentrations in CF children. METHODS: A cross-sectional study with 26 CF children aged 5.0-15.5 years and 33 healthy controls, mean age 9.4 years. Body composition was evaluated by dual-energy X-ray absorptiometry. Fasting blood samples were analyzed for leptin, IGF-1 and IGFBP-3. RESULTS: FBM standard deviation score (SDS; CF boys -0.02 +/- 0.88 vs. 0.78 +/- 0.65, p < 0.01; CF girls -0.37 +/- 1.15 vs. 0.70 +/- 0.97, p < 0.05), leptin concentration (CF boys 2.07 +/- 0.79 vs. 3.07 +/- 1.28 ng/ml, p < 0.05; CF girls 2.71 +/- 0.86 vs. 5.00 +/- 2.95 ng/ml, p < 0.05) and IGF-1SDS (CF boys -1.43 +/- 1.50 vs. -0.32 +/- 0.88, p < 0.05; CF girls -0.66 +/- 1.66 vs. 0.64 +/- 0.57, p < 0.01) were lower in CF children compared to controls. Shwachman score was the strongest predictor of lean body mass (R = 0.63). Leptin levels explain 60% of the variability in FBM. CONCLUSION: Serum concentrations of IGF-1 and leptin are decreased in children with CF and are associated with clinical conditions and body composition.
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| 4. |
- Bruett, Anna Levke, et al.
(author)
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Assessment of Health-Related Quality of Life and Patient Satisfaction in Children and Adolescents with Growth Hormone Deficiency or Idiopathic Short Stature - Part 1 : A Critical Evaluation of Available Tools
- 2009
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In: Hormone Research. - : S. Karger AG. - 0301-0163 .- 1423-0046. ; 72:2, s. 65-73
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Research review (peer-reviewed)abstract
- The concept of health-related quality of life (HrQoL) reflects the subjective perception of health and includes aspects of well-being and functioning in physical, emotional, mental and social life domains. Nowadays, HrQoL has become a relevant treatment outcome from epidemiological and clinical perspectives and is also broadly employed in health economic analyses. To assess HrQoL generic as well as condition-specific instruments are used. The former are applicable to a wide range of health conditions and aim at measuring HrQoL across different conditions. The latter focus on capturing the impact of a specific disease. Although HrQoL research in adults is now well-advanced, there are still open questions regarding how to assess HrQoL in pediatric conditions, such as short stature. Eight generic (one chronic-generic) and seven condition-specific (one treatment-specific) instruments used in HrQoL research in short stature of youth are described. Additionally, this mini review identifies a need for further research and indicates potential directions.
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| 5. |
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| 6. |
- Chagin, AS, et al.
(author)
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Androgen receptor modulation does not affect longitudinal growth of cultured fetal rat metatarsal bones
- 2009
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In: Hormone research. - : S. Karger AG. - 1423-0046. ; 71:4, s. 219-227
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Journal article (peer-reviewed)abstract
- <i>Background:</i> Systemic administration of the nonaromatizable androgen oxandrolone stimulates growth in girls with Turner syndrome and boys with a constitutional delay of growth and puberty. It is unknown if oxandrolone acts locally at the growth plate level to stimulate longitudinal bone growth. <i>Methods:</i> Metatarsal bones from female and male rat fetuses (day E20) were cultured for 14 days in the presence of oxandrolone, testosterone or the androgen receptor (AR) antagonist flutamide with/without insulin-like growth-factor-I (IGF-I) or charcoal-treated serum. <i>Results:</i> The AR was found to be expressed in both male and female fetal rat metatarsal bones. Neither oxandrolone nor testosterone had any effect on metatarsal bone growth when tested at a wide concentration range (1 n<i>M</i> to 10 μ<i>M</i>), not even in the presence of IGF-I (100 ng/ml) or charcoal-treated serum (10%). Bone growth was also unaffected when the AR was blocked by flutamide. Control experiments confirmed that metatarsal bone growth was significantly stimulated by IGF-I (p < 0.001). <i>Conclusion:</i> Modulation of AR activity in the fetal rat growth plate does not affect linear bone growth. Extrapolating from these in vitro data, it could be speculated that oxandrolone stimulates longitudinal bone growth in treated children by acting indirectly rather than directly through AR activation in growth plate chondrocytes.
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| 7. |
- Chagin, AS, et al.
(author)
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Genes of importance in the hormonal regulation of growth plate cartilage
- 2009
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In: Hormone research. - : S. Karger AG. - 1423-0046. ; 7171 Suppl 2, s. 41-47
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Journal article (peer-reviewed)abstract
- Longitudinal bone growth occurs in the growth plate through a process in which resting zone chondrocytes are recruited to start active proliferation and then undergo differentiation, followed by apoptosis and later mineralization. Bone growth is controlled by a multitude of genes encoding for hormones and growth factors acting systemically and/or locally in the growth plate. From studies of individuals with a mutated aromatase gene and a male patient with defective oestrogen receptor (ER) α, it has become clear that the action of oestrogen is indispensable for normal pubertal growth and growth plate fusion. As new aromatase inhibitors and specific modulators of ERs are developed, these could offer more specific ways to modulate longitudinal growth and growth plate fusion. It is difficult to extrapolate data obtained in experimental animals, as clear species differences exist, emphasizing the need for new models that will allow studies in human growth plate cartilage.
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| 8. |
- Christesen, Henrik B. T., et al.
(author)
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Rapid genetic analysis in congenital hyperinsulinism
- 2007
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In: Hormone Research. - : S. Karger AG. - 0301-0163. ; 67:4, s. 184-188
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Journal article (peer-reviewed)abstract
- Backgound: In severe, medically unresponsive congenital hyperinsulinism (CHI), the histological differentiation of focal versus diffuse disease is vital, since the surgical management is completely different. Genetic analysis may help in the differential diagnosis, as focal CHI is associated with a paternal germline ABCC8 or KCNJ11 mutation and a focal loss of maternal chromosome 11p15, whereas a maternal mutation, or homozygous/compound heterozygous ABCC8 and KCNJ11 mutations predict diffuse-type disease. However, genotyping usually takes too long to be helpful in the absence of a founder mutation. Methods: In 4 patients, a rapid genetic analysis of the ABBC8 and KCNJ11 genes was performed within 2 weeks on request prior to the decision of pancreatic surgery. Results: Two patients had no mutations, rendering the genetic analysis non-informative. Peroperative multiple biopsies showed diffuse disease. One patient had a paternal KCNJ11 mutation and focal disease confirmed by positron emission tomography scan and biopsies. One patient had a de novo heterozygous ABBC8 mutation and unexplained diffuse disease confirmed by positron emission tomography scan and biopsies. Conclusion: A rapid analysis of the entire ABBC8 and KCNJ11 genes should not stand alone in the preoperative assessment of patients with CHI, except for the case of maternal, or homozygous/compound heterozygous disease-causing mutations. Copyright (c) 2007 S. Karger AG, Basel.
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| 9. |
- Domene, HM, et al.
(author)
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Human acid-labile subunit deficiency: clinical, endocrine and metabolic consequences
- 2009
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In: Hormone research. - : S. Karger AG. - 1423-0046. ; 72:3, s. 129-141
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Journal article (peer-reviewed)abstract
- The majority of insulin-like growth factor (IGF)-I and IGF-II circulate in the serum as a complex with the insulin-like growth factor binding protein (IGFBP)-3 or IGFBP-5, and an acid-labile subunit (ALS). The function of ALS is to prolong the half-life of the IGF-I-IGFBP-3/IGFBP-5 binary complexes. Fourteen different mutations of the human <i>IGFALS</i> gene have been identified in 17 patients, suggesting that ALS deficiency may be prevalent in a subset of patients with extraordinarily low serum levels of IGF-I and IGFBP-3 that remain abnormally low upon growth hormone stimulation. Postnatal growth was clearly affected. Commonly, the height standard deviation score before puberty was between –2 and –3, and approximately 1.4 SD shorter than the midparental height SDS. Pubertal delay was found in 50% of the patients. Circulating IGF-II, IGFBP-1, -2 and -3 levels were reduced, with the greatest reduction observed for IGFBP-3. Insulin insensitivity was a common finding, and some patients presented low bone mineral density. Human ALS deficiency represents a unique condition in which the lack of ALS proteins results in the disruption of the entire IGF circulating system. Despite a profound circulating IGF-I deficiency, there is only a mild impact on postnatal growth. The preserved expression of locally produced IGF-I might be responsible for the preservation of linear growth near normal limits.
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| 10. |
- Groop, Leif, et al.
(author)
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Insulin sensitivity in adults with growth hormone deficiency and effect of growth hormone treatment.
- 2005
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In: Hormone Research. - : S. Karger AG. - 0301-0163. ; 64:Suppl 3, s. 45-50
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Journal article (peer-reviewed)abstract
- Adult growth hormone deficiency (GHD) is a multifactorial disorder in which pituitary dysfunction associated with pituitary adenomas or their treatment plays a major role. The introduction of recombinant growth hormone (GH) for the treatment of GHD has opened up new treatment avenues but has also raised concerns about possible untoward long-term metabolic effects of GH, such as the potential effect of GH on insulin sensitivity and a deterioration in glucose tolerance. Research has shown that GH induces insulin resistance by the stimulation of lipolysis and a concomitant switch from oxidation of glucose to oxidation of lipids, during both acute and chronic treatment. However, although this is a consistent effect of GH therapy, it does not mean per se that it leads to abnormal glucose tolerance and diabetes mellitus. This article discusses this and other potential long-term metabolic effects of GH, and raises a number of questions to be addressed by future research.
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| 11. |
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| 12. |
- Hoybye, C
(author)
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Inflammatory markers in adults with Prader-Willi syndrome before and during 12 months growth hormone treatment
- 2006
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In: Hormone research. - : S. Karger AG. - 0301-0163. ; 66:1, s. 27-32
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Journal article (peer-reviewed)abstract
- <i>Background:</i> In Prader-Willi syndrome (PWS) obesity and partial growth hormone (GH) deficiency are frequently observed. The risks of cardiovascular diseases and early death are increased. We examined inflammatory markers in adult PWS, before and during 12 months of GH treatment. <i>Method:</i> Twelve PWS adults, median age 23.5 years (17–37) and median BMI 33.8 kg/m<sup>2</sup> (21.2–50.4), participated. Serum interleukin-6, tumour necrosis factor α, high sensitive protein C-reactive protein (HCRP), cholesterol, triglycerides, leptin, adiponectin, glucose, insulin, insulin-like growth factor I and body composition were measured at baseline and after 6 and 12 months of GH treatment. <i>Results:</i> Median and range at baseline for interleukin-6 was 9.87 ng/l (1.76–10.72), for tumour necrosis factor α 2.39 ng/l (1.00–3.26) and for HCRP 7.64 mg/l (0.41–41.1) (normal values < 5 ng/l, < 8 ng/l and<5 mg/l, respectively). At baseline correlations between inflammatory markers and age, anthropometry, body composition and the metabolic parameters were non-significant; only positive associations were found between tumour necrosis factor α and body weight (r = 0.617, p = 0.033) and between HCRP and BMI (r = 0.594, p = 0.041). GH treatment non-significantly decreased the levels of the inflammatory markers. <i>Conclusion:</i> In this pilot study, levels of interleukin-6 and HCRP were increased, and GH intervention did not significantly reduce the levels. Chronic inflammation might contribute to the increased cardiovascular morbidity and mortality in PWS.
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| 13. |
- Johannsson, Gudmundur, 1960, et al.
(author)
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Long-acting hydrocortisone for glucocorticoid replacement therapy.
- 2007
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In: Hormone research. - : S. Karger AG. - 1423-0046 .- 0301-0163. ; 68 Suppl 5, s. 182-8
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Journal article (peer-reviewed)abstract
- BACKGROUND: Glucocorticoid (GC) deficiency is a consequence of various disorders that are by themselves rare. Because of this low prevalence, the low cost of GC replacement therapy and the belief that existing outcomes are good, there has been little interest in development of new and improved pharmaceutical products for treatment of GC deficiency. However, GC replacement therapy is complex: diurnal variation of endogenous cortisol must be replicated, GC needs may change during times of physical and psychological stress and there is no biomarker of its action that can be used to monitor individual dose response. CURRENT LIMITATIONS: Recent data suggest that the outcome of established long-term GC replacement therapy may not be as good as previously believed. Short-acting GCs such as hydrocortisone (HC) and cortisone acetate for replacement therapy require 2 to 3 administrations per day. DEVELOPING ALTERNATIVES: Drug delivery system technologies are now available that could permit design and manufacture of a formulation that could accommodate once-daily administration of HC. Such a formulation would enable more physiological serum cortisol-time profiles than are possible with currently available formulations. This short review provides some background on GC replacement therapy, along with recent data on the outcome of patient groups with GC insufficiency, and briefly discusses some general principles for a controlled-release ('long-acting') HC formulation.
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| 14. |
- Johannsson, Gudmundur, 1960
(author)
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Treatment of growth hormone deficiency in adults.
- 2009
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In: Hormone research. - : S. Karger AG. - 1423-0046. ; 71 Suppl 1, s. 116-22
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Journal article (peer-reviewed)abstract
- BACKGROUND: The Growth Hormone Research Society held a Consensus Workshop in Sydney, Australia, in March 2007 to review advances in the management of growth hormone (GH) deficiency in adults and to update consensus recommendations. OBJECTIVE: This short review summarizes key background information presented at the workshop and the consensus recommendations that followed. CONCLUSIONS: The benefits of GH replacement in GH-deficient adults are evident throughout life. Clinical response to treatment should be assessed by monitoring biochemistry values, body composition and quality of life. There is no evidence that GH replacement increases the risk of tumour recurrence or de novo malignancy.
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| 15. |
- Kugelberg, Maria, et al.
(author)
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Reduced bone mineral density and radial bone growth in young rabbits treated with dexamethasone eye drops.
- 2005
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In: Hormone research. - : S. Karger AG. - 0301-0163. ; 63:4, s. 165-70
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Journal article (peer-reviewed)abstract
- OBJECTIVE: To investigate the effect of dexamethasone eye drops on bone metabolism in newborn rabbits. METHODS: Thirty-four 3-week-old rabbits had unilateral clear lens extraction and were randomized into three groups. Postoperatively, group 1 received high-dose and group 2 low-dose dexamethasone eye drops (average doses 0.27 and 0.10 mg/kg body weight/day, respectively). These rabbits also received a postoperative subconjunctival injection of betamethasone. Group 3 (control) received vehicle eye drops only. After 8 weeks of treatment, all animals were killed and the left femurs were isolated and subjected to peripheral quantitative computerized tomography (pQCT) and dual X-ray absorptiometry (DXA) analyses. RESULTS: DXA showed that rabbits treated with either a high or low dose of dexamethasone eye drops had significantly reduced areal bone mineral density (BMD), area and total bone mineral content (BMC) of the femur. Measurements with pQCT demonstrated a dose-dependent reduction in cortical BMC, cortical volumetric BMD and cortical area. These effects were associated with an inhibition of radial femur growth, cortical thickness and periosteal and endosteal circumferences. CONCLUSION: Dexamethasone eye drops have systemic effects affecting several bone parameters in young rabbits. Any long-term systemic effects of ocular glucocorticoids need to be further studied.
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| 16. |
- Mottagui-Tabar, S, et al.
(author)
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Association of ADRB1 and UCP3 gene polymorphisms with insulin sensitivity but not obesity
- 2008
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In: Hormone research. - : S. Karger AG. - 1423-0046. ; 69:1, s. 31-36
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Journal article (peer-reviewed)abstract
- <i>Background:</i> The uncoupling proteins (UCPs) and β-adrenoceptors (ADRBs) are important for energy balance and may be involved in the pathogenesis of insulin resistance. Obesity is strongly hunted by insulin resistance and susceptibility genes for the two conditions could be separate or common. Variations within the <i>UCPs </i>and <i>ADRBs </i>genes may give important clues to their involvement in disease. <i>Methods:</i> A total of four single nucleotide polymorphisms (SNPs) in the genes <i>UCP1, UCP2, UCP3, and ADRB1</i> were examined for association with obesity and insulin sensitivity (HOMA<sub>IR</sub>) in obese (n = 292) and healthy non-obese (n = 481) females. <i>Results:</i> None of the SNPs was associated with obesity status or body mass index. However, <i>ADRB1 </i>(rs1801253) was nominally associated with serum insulin (nominal p = 0.034) and HOMA<sub>IR</sub> (nominal p = 0.022). <i>UCP3</i> (rs1800006) was in post-hoc analysis nominally associated with serum insulin and HOMA<sub>IR</sub> (nominal p = 0.013 and 0.048, respectively).<i> UCP1 </i>and <i>UCP2</i> showed no association with insulin sensitivity. <i>Conclusion:</i> Polymorphisms in <i>ADRB1</i> and <i>UCP3</i> may contribute to insulin resistance rather than obesity among Swedish women.
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| 17. |
- Nilsson, O, et al.
(author)
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Endocrine regulation of the growth plate
- 2005
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In: Hormone research. - : S. Karger AG. - 0301-0163. ; 64:4, s. 157-165
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Journal article (peer-reviewed)abstract
- Longitudinal bone growth occurs at the growth plate by endochondral ossification. Within the growth plate, chondrocyte proliferation, hypertrophy, and cartilage matrix secretion result in chondrogenesis. The newly formed cartilage is invaded by blood vessels and bone cells that remodel the newly formed cartilage into bone tissue. This process of longitudinal bone growth is governed by a complex network of endocrine signals, including growth hormone, insulin-like growth factor I, glucocorticoid, thyroid hormone, estrogen, androgen, vitamin D, and leptin. Many of these signals regulate growth plate function, both by acting locally on growth plate chondrocytes and also indirectly by modulating other endocrine signals in the network. Some of the local effects of hormones are mediated by changes in paracrine factors that control chondrocyte proliferation and differentiation. Many human skeletal growth disorders are caused by abnormalities in the endocrine regulation of the growth plate. This review provides an overview of the endocrine signals that regulate longitudinal bone growth, their interactions, and the mechanisms by which they affect growth plate chondrogenesis.
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| 18. |
- Nordenstroem, A, et al.
(author)
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A case of 3beta-hydroxysteroid dehydrogenase type II (HSD3B2) deficiency picked up by neonatal screening for 21-hydroxylase deficiency: difficulties and delay in etiologic diagnosis
- 2007
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In: Hormone research. - : S. Karger AG. - 1423-0046. ; 68:4, s. 204-208
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Journal article (peer-reviewed)abstract
- <i>Background:</i> 3β-Hydroxysteroid dehydrogenase type II deficiency, a rare form of congenital adrenal hyperplasia, is characterized by varying degrees of salt loss and incomplete masculinization in males and mild virilization or normal external genitalia in females. The clinical signs may be difficult to recognize, increasing the risk of a neonatal adrenal crisis. In addition, elevated 17α-hydroxyprogesterone and androstenedione levels due to peripheral HSD3B1 activity may lead to a delay of the correct diagnosis and even to misdiagnosis as CYP21 deficiency. <i>Method:</i> We report a patient who was detected on neonatal screening for 21-hydroxylase deficiency, in part because of cross-reactivity in the commonly used assay. <i>Results:</i> The diagnostic difficulties in this case were overcome by the use of more specific antibodies. <i>Conclusion:</i> This case emphasizes the importance of confirming the etiological diagnosis with molecular genetic analyses.
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| 19. |
- Nordenstrom, A, et al.
(author)
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Female preponderance in congenital adrenal hyperplasia due to CYP21 deficiency in England: implications for neonatal screening
- 2005
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In: Hormone research. - : S. Karger AG. - 0301-0163. ; 63:1, s. 22-28
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Journal article (peer-reviewed)abstract
- Congenital adrenal hyperplasia (CAH) due to 21-hydroxylase (CYP21) deficiency causes symptoms ranging from life-threatening neonatal adrenal crises to minimal virilization in adulthood. The relationship between <i>CYP21</i> genotype and phenotypic markers in a non-screened population of 73 CAH children (44 female, 29 male; 54 white, 19 Asian) treated at the Royal Manchester Children’s Hospital was investigated and ethnic and sex differences assessed. The patients were categorized according to the mutation on the mildest allele. The age at the time of diagnosis differed significantly between the groups (p = 0.02): all 25 Null and 25 of 26 of the I2 splice patients were diagnosed during the neonatal period, whereas 7 of 11 I172N patients were diagnosed late. Degree of female genital virilization, 17-hydroxyprogesterone level at diagnosis, and fludrocortisone requirement during the 1st year of treatment correlated with the genotype, although Asian Null patients required more fludrocortisone than their white counterparts (p = 0.055). There was an equal sex ratio in both the I2 splice (12 female/14 male) and I172N (5 female/6 male) groups. However, in the Null group, the ratio was 4.0 (20 female/5 male; p = 0.003), suggesting that some Null male infants perish before being clinically detected to have CYP21 deficiency. Our findings strongly support the need for implementation of a neonatal screening programme for CAH in the UK which may reduce the male infant mortality.
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| 20. |
- Nwosu, BU, et al.
(author)
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Lack of telomere shortening with age in mouse resting zone chondrocytes
- 2005
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In: Hormone research. - : S. Karger AG. - 0301-0163. ; 63:3, s. 125-128
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Journal article (peer-reviewed)abstract
- <i>Background and Aim:</i> Telomeres are hexameric repeat sequences that flank eukaryotic chromosomes. The telomere hypothesis of cellular aging proposes that replication of normal somatic cells leads to progressive telomere shortening which induces replicative senescence. Previous studies suggest that growth plate chondrocytes have a finite proliferative capacity in vivo. We therefore hypothesized that telomere shortening in resting zone chondrocytes leads to replicative senescence. <i>Method:</i> To test this hypothesis we compared the telomere restriction fragment (TRF) length of <i>Mus casteneus</i> at 1, 4, 8, and 56 weeks of age. <i>Results and Conclusions:</i> We found that TRF length did not diminish measurably with age, suggesting that telomere shortening in resting zone chondrocytes is not the mechanism that limits proliferation of growth plate chondrocytes in vivo.
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| 21. |
- Olausson, Hanna, 1975-, et al.
(author)
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Longitudinal study of the maternal insulin-like growth factor system before, during and after pregnancy in relation to fetal and infant weight
- 2008
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In: Hormone Research. - : S. Karger AG. - 0301-0163 .- 1423-0046. ; 69:2, s. 99-106
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Journal article (peer-reviewed)abstract
- Background: The maternal insulin-like growth factor (IGF) system is considered to be involved in fetal growth regulation. However, available data linking this system to fetal growth are contradictory and incomplete.Aims: To measure components of the IGF system before, during and after pregnancy in healthy women and to relate these results, and their changes during pregnancy, to fetal weight (gestational week 31) and birth weight.Methods: Serum concentrations of IGF-I, IGF-II, IGF-binding protein (IGFBP)-1, IGFBP-3 and IGFBP-3 protease activity were assessed in 23 women before conception, at weeks 8, 14, 20, 32 and 35 of pregnancy and 2 weeks postpartum. The data were analyzed using simple and multiple linear regression.Results: One third of the variability in fetal weight was explained by IGF-I in combination with IGFBP-3 protease activity, both assessed at gestational week 32 (p = 0.013). Birth weight was negatively correlated (r = –0.43 to –0.59) with IGFBP-1 at gestational week 20 (p = 0.041), 32 (p = 0.012) and 35 (p = 0.003).Conclusion: We propose there is a finely tuned balance among the components of the IGF system, providing a means for fetal growth regulation.
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| 22. |
- Padidela, R, et al.
(author)
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Abnormal growth in noonan syndrome: genetic and endocrine features and optimal treatment
- 2008
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In: Hormone research. - : S. Karger AG. - 1423-0046. ; 70:3, s. 129-136
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Journal article (peer-reviewed)abstract
- Noonan syndrome (NS) is a phenotypically heterogeneous syndrome which is frequently associated with short stature. Recent genetic investigations have identified mutations in five genes, namely PTPN11, KRAS, SOS1, NF1 and RAF1 in patients with the NS phenotype. PTPN11 is the commonest, being present in approximately 50% of cases. The degree of short stature in children does not associate closely with the presence of mutations, however some PTPN11-positive patients have decreased GH-dependent growth factors consistent with mild GH insensitivity. GH therapy, using doses similar to those approved for Turner syndrome (TS), induced short-term increases in height velocity over 1–3 years, and may improve final adult height with longer-term treatment.
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| 23. |
- Petersen, C, et al.
(author)
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The sertoli cell--a hormonal target and 'super' nurse for germ cells that determines testicular size
- 2006
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In: Hormone research. - : S. Karger AG. - 0301-0163. ; 66:4, s. 153-161
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Journal article (peer-reviewed)abstract
- The somatic Sertoli cell plays an essential role in embryonic determination of male somatic sex and in spermatogenesis during adult life. One individual Sertoli cell supplies a clone of developing germ cells with nutrients and growth factors and it is well established that the number of Sertoli cells present is closely correlated to both testicular size and sperm output. Sertoli cells continue to proliferate and differentiate until the beginning of puberty, when they cease dividing and start nursing the germ cells. At this point in time, the future capacity of the testis for sperm production has thus been determined. Prior to puberty the Sertoli cells are immature and differ considerably with respect to morphology and biochemical activity from the mature cell. The several investigations that have focused on hormonal and paracrine regulation of the functions of the mature cell are reviewed here, but the mechanisms underlying the maturation and general maintenance of well-functioning Sertoli cells remain obscure. An alarming decline in male reproductive health has been observed in several Western countries during recent decades. Disturbance of Sertoli cell differentiation is thought to be involved in the pathogenesis of both a poor sperm count and testicular cancer. It is speculated that environmental agents that disrupt the estrogenic/androgenic balance in the testis may play a role in this connection.
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| 24. |
- Pihl, S, et al.
(author)
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Acute interleukin-6 infusion increases IGFBP-1 but has no short-term effect on IGFBP-3 proteolysis in healthy men
- 2006
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In: Hormone research. - : S. Karger AG. - 0301-0163. ; 65:4, s. 177-184
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Journal article (peer-reviewed)abstract
- Human conditions of elevated interleukin-6 (IL-6) and transgenic mice overexpressing IL-6 have increased proteolytic degradation of insulin-like growth factor binding protein (IGFBP)-3. In addition, IL-6 alters the hepatic expression of insulin-like growth factor-I (IGF-I) and the IGFBPs in vitro. The aim of the present study was to investigate whether moderately elevated IL-6 levels have short-term effects on circulating IGF-I, IGFBP-1 and IGFBP-3 proteolysis in vivo. Healthy men received a 3-h IL-6 (n = 6) or saline (n = 6) infusion and blood samples were collected prior to and up to 8 h after the start of infusion. Free IGF-I, total IGF-I, IGFBP-1, insulin and cortisol were measured using immunoassays. Serum IGFBP-3 proteolysis was analyzed by Western immunoblot and by in vitro degradation of <sup>125</sup>I-IGFBP-3. We found that IL-6 concentrations reaching approximately 100 pg/ml significantly increased IGFBP-1 after the end of infusion in the absence of changes in insulin. In addition, plasma levels of cortisol were increased in response to IL-6 during and after infusion compared to saline. There was no effect of IL-6 on IGFBP-3 proteolysis, total IGF-I or free dissociable IGF-I. These data suggest that moderately elevated levels of IL-6 such as in the post-operative state or after exercise may contribute to increased levels of IGFBP-1. Although this study does not exclude that high levels and/or prolonged exposure to IL-6 may induce IGFBP-3 proteolysis in sepsis or chronic inflammatory disease, it suggests that IL-6 released from exercising skeletal muscle is not directly involved in proteolysis of circulating IGFBP-3.
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| 25. |
- Ranke, M. B., et al.
(author)
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Age at Growth Hormone Therapy Start and First-Year Responsiveness to Growth Hormone Are Major Determinants of Height Outcome in Idiopathic Short Stature
- 2007
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In: Horm Res. - : S. Karger AG. - 0301-0163. ; 68:2, s. 53-62
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Journal article (peer-reviewed)abstract
- Aim: To develop methods to identify factors associated with a favorable outcome in GH-treated children with idiopathic short stature (ISS). Methods: From 4,685 children listed as having ISS within KIGS (Pfizer International Growth Database), we studied (a) the prediction model group (n = 657) to develop the first-year prediction model, and (b) the near adult height group (NAH; n = 256) which received GH for >4 years to develop descriptive models for adult height and overall height gain. Results: NAH group at GH start: age was 10.0 years, height -2.5 SD score (SDS), weight -2.3 SDS, height minus mid-parental height (MPH) -1.5 SDS; GH dose 0.19 mg/kg/week. Height gain was 1.1 SDS at a median age of 17.2 years. Growth response correlated positively with GH dose and weight at the start of GH treatment, and negatively with age and height SDS minus MPH SDS. The model explains 39% (error SD 1.2 cm) of the variability. Adult height correlated (R(2) = 0.64) positively with height at GH start, MPH and the first-year responsiveness to GH, and negatively with age. Conclusions: Prepubertal children with ISS who show an appropriate first-year response to GH are likely to benefit from long-term treatment, even on low GH dosages. Copyright (c) 2007 S. Karger AG, Basel.
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| 26. |
- Savendahl, L
(author)
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Hormonal regulation of growth plate cartilage
- 2005
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In: Hormone research. - : S. Karger AG. - 0301-0163. ; 6464 Suppl 2, s. 94-97
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Journal article (peer-reviewed)abstract
- Longitudinal bone growth occurs in the growth plate through a process called endochondral bone formation, a process where resting zone chondrocytes are recruited to start active proliferation and then undergo differentiation, followed by apoptosis and later mineralization. The balance between proliferation and differentiation is a crucial regulatory step controlled by various growth factors/hormones acting in both endocrine and paracrine/autocrine ways. From studies of individuals with aromatase deficiency and a boy with defective oestrogen receptor (ER)-alpha it has become clear that oestrogen action is indispensable for normal pubertal growth and growth plate fusion. Both oestrogen receptors, ER-alpha and ER-beta, are expressed in the growth plate in boys and girls throughout pubertal development. Any functional role of ER-beta has not yet been defined in the human growth plate. Increased understanding about the effects of oestrogen and the interactions between oestrogens and other endocrine factors within the growth plate is important for the development of new treatment strategies in different disorders affecting longitudinal bone growth. As new specific modulators of oestrogen receptors are developed, these could offer more specific ways to modulate longitudinal growth and growth plate fusion.
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| 27. |
- Sigurjónsdóttir, Helga A, 1964, et al.
(author)
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Liquorice in moderate doses does not affect sex steroid hormones of biological importance although the effect differs between the genders.
- 2006
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In: Hormone research. - : S. Karger AG. - 0301-0163. ; 65:2, s. 106-10
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Journal article (peer-reviewed)abstract
- BACKGROUND/AIM: Liquorice is commonly consumed, at least in the western world, and we have earlier shown that even moderate doses of liquorice have significant effects on the cortisol metabolism by inhibiting 11beta-hydroxysteroid dehydrogenase type 2. The suggestion that liquorice decreases the testosterone levels in men makes it vital to study the effect of moderate doses of liquorice on sex steroid hormones. METHODS: Fifteen women and 21 men (healthy volunteers and subjects with essential hypertension) consumed 100 g of liquorice (150 mg glycyrrhetinic acid) daily in a 9-week, open-treatment trial. Blood and 24-hour urine samples were collected for hormone analysis before and after 4 weeks of liquorice consumption and 4 weeks after cessation of liquorice intake. RESULTS: The liquorice induced a moderate decrease in the serum concentrations of dehydroepiandrostenedione sulphate in men (p = 0.002). The relative change in serum levels of dehydroepiandrosterone sulphate differed between the genders (p = 0.03). No significant changes were observed in the serum testosterone levels after 4 weeks of liquorice consumption, and the urine excretion of androgens (etiocholanolone and androstenedione) did not change. CONCLUSIONS: Liquorice in moderate doses primarily affects the cortisol metabolism and only marginally the androgen hormones. Gender may influence the action of liquorice.
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| 28. |
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| 29. |
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| 30. |
- Supornsilchai, V, et al.
(author)
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Phytoestrogen resveratrol suppresses steroidogenesis by rat adrenocortical cells by inhibiting cytochrome P450 c21-hydroxylase
- 2005
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In: Hormone research. - : S. Karger AG. - 0301-0163. ; 64:6, s. 280-286
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Journal article (peer-reviewed)abstract
- <i>Background and Aim:</i> The phytoestrogen resveratrol is found in grapes, mulberries and peanuts, all of which are consumed regularly by humans. Resveratrol is also used in chemotherapy against cancer and aging and as a cardioprotectant. The aim of the present study was to characterize the effects of resveratrol on rat adrenal steroidogenesis and to study the underlying mechanism. <i>Methods: </i>Adrenocortical cells were isolated from the adrenal glands of normal male rats (in vitro) and from male rats administered resveratrol in their diet for 12 weeks (ex vivo). Cells from resveratrol-treated and non-treated rats were tested ex vivo for responsiveness to ACTH and cells from normal rats were tested in vitro for responsiveness to ACTH in the presence and absence of resveratrol. Corticosterone and progesterone production were measured by RIA and expression of steroidogenic enzymes analyzed by PAGE/Western blotting. <i>Results:</i> Corticosterone production was inhibited 47% by 50 µ<i>M</i> resveratrol in vitro and 20% ex vivo, while progesterone production was elevated to 400% of the control value in in vitro experiments. Resveratrol treatment decreased adrenal cytochrome P450 c21-hydroxylase expression in vivo and cell culture conditions. No changes in cell viability or morphology were caused by exposure to resveratrol in both ex vivo and in vitro experiments. <i>Conclusion:</i> Resveratrol suppresses corticosterone production by primary rat adrenocortical cell cultures in vitro and ex vivo by inhibiting cytochrome P450 c21-hydroxylase.
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| 31. |
- Swenne, Ingemar, et al.
(author)
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Triiodothyronine Is an Indicator of Nutritional Status in Adolescent Girls with Eating Disorders
- 2009
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In: Hormone Research. - : S. Karger AG. - 0301-0163 .- 1423-0046. ; 71:5, s. 268-275
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Journal article (peer-reviewed)abstract
- Aim: Circulating thyroid hormone concentrations are influenced by nonthyroidal disease and changes in nutritional status. We studied thyroid hormones as possible indicators of nutrition in adolescent girls with eating disorders. Method: Blood samples for analyses of thyroid hormones were obtained at 360 assessments of 298 patients and biweekly during 42 treatment periods in 36 patients. Results: At assessment, when most of the girls were on a weight losing course, serum triiodothyronine (T3) concentrations were low. Great weight loss and rapid rate of weight loss were the most important predictors of low T3 concentrations. Serum free thyroxine concentrations were in the lower normal range. In premenarcheal girls, weight loss was the most important predictor of free thyroxine but this relationship was weaker in postmenarcheal girls. Serum TSH concentrations were within the normal range and only weakly related to weight changes. During treatment, T3 increased in parallel with weight but was also influenced by the short-term weight trend. Conclusion: Serum T3 concentration is an indicator of nutritional status in adolescent girls with eating disorders. It is sensitive to short-term weight changes and could be used to monitor progress throughout nutritional rehabilitation.
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| 32. |
- Swenne, Ingemar
(author)
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Weight and growth requirements for menarche in teenage girls with eating disorders, weight loss and primary amenorrhea
- 2008
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In: Hormone Research. - : S. Karger AG. - 0301-0163 .- 1423-0046. ; 69:3, s. 146-151
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Journal article (peer-reviewed)abstract
- BACKGROUND/AIM: To investigate weight and growth requirements for menarche in girls with eating disorders (ED), weight loss and primary amenorrhea. METHODS: Growth charts from school health services and measurements of weight and stature throughout treatment were obtained for 47 such girls. RESULTS: Weight loss started at an age of 12.4 +/- 1.6 years from a top weight of 41.7 +/- 7.1 kg. Approximately a year later they had lost 5.1 +/- 4.3 kg and grown only 2.8 +/- 3.5 cm. Following treatment and weight gain, growth accelerated and the girls reached a peak growth velocity of 4.3 +/- 2.6 cm/year 2 years before menarche which occurred at an age of 15.5 +/- 1.6 years at a weight of 52.2 +/- 5.3 kg. Menarche occurred within a wide range of weights but could be predicted by a linear regression on prepubertal weight (R(2) = 0.39; p < 0.001). CONCLUSIONS: Following treatment, girls with ED and primary amenorrhea progress through puberty at a slowed rate. The weight required for menarche can be predicted by the prepubertal weight which may represent the individual's normal growth track unaffected by the ED.
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| 33. |
- Van Cauter, Eve, et al.
(author)
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Impact of sleep and sleep loss on neuroendocrine and metabolic function
- 2007
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In: Hormone Research. - : S. Karger AG. - 0301-0163 .- 1423-0046. ; 67:Suppl. 1, s. 2-9
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Journal article (peer-reviewed)abstract
- Background: Sleep exerts important modulatory effects on neuroendocrine function and glucose regulation. During the past few decades, sleep curtailment has become a very common behavior in industrialized countries. This trend toward shorter sleep times has occurred over the same time period as the dramatic increases in the prevalence of obesity and diabetes. Aims: This article will review rapidly accumulating laboratory and epidemiologic evidence indicating that chronic partial sleep loss could play a role in the current epidemics of obesity and diabetes. Conclusions: Laboratory studies in healthy young volunteers have shown that experimental sleep restriction is associated with a dysregulation of the neuroendocrine control of appetite consistent with increased hunger and with alterations in parameters of glucose tolerance suggestive of an increased risk of diabetes. Epidemiologic findings in both children and adults are consistent with the laboratory data.
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| 34. |
- Westphal, Otto, 1935
(author)
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Growth hormone therapy in Noonan syndrome: growth response and characteristics.
- 2009
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In: Hormone research. - : S. Karger AG. - 1423-0046. ; 72:Suppl 2, s. 41-5
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Journal article (peer-reviewed)abstract
- Growth hormone treatment in Noonan syndrome increases growth velocity significantly during the first 2 years of treatment and, to some extent, until puberty. This increase is more pronounced if treatment is started at an early age. Treatment before the age of 5 years is not recommended due to an increased risk of malignancies. In contrast to other growth hormone-treated patients, a slight but significant further increase in height gain can be expected during pubertal growth (at least in boys). Final height improvement varies between 1 and 2 SDS in different studies. Cardiac function does not seem to be impaired during treatment. No significant adverse events have been reported.
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