Plasma Growth hormone (GH)-binding proteins: effect on GH binding to receptors and GH action

Mannor, Dana A.; Winer, Lori M.; Shaw, Melissa A.; Baumann, Gerhard

doi:10.1007/bf00878369

Cited by 18 publications

(22 citation statements)

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“…The differences in the developmental patterns of the GHBP and GHR mRNA in kidney and lung may also indicate differential regulation of the two transcripts in a more physiologic model. Although their functional interplay is not understood, the GHBP may compete with the GHR for GH binding (5,6). The GHBP, therefore, might serve as a storage protein that smooths out the pulsatile exposure of cells to GH and thereby regulates the availability of GH to the membrane-bound receptor (6).…”

Section: Liver Kidney Ileum Lungmentioning

confidence: 99%

“…Although their functional interplay is not understood, the GHBP may compete with the GHR for GH binding (5,6). The GHBP, therefore, might serve as a storage protein that smooths out the pulsatile exposure of cells to GH and thereby regulates the availability of GH to the membrane-bound receptor (6). Clearance of GH from the circulation takes place largely in the kidney by glomerular filtration, followed by resorption in the proximal tubule and degradation (26).…”

Section: Liver Kidney Ileum Lungmentioning

confidence: 99%

“…The soluble GHR, the GHBP, appears to be an alternatively spliced product of the GHR gene in rats (4) that is composed of the extracellular domain of the GHR but that has a unique 17-amino acid hydrophilic tail instead of the transmembrane and intracellular domains of the receptor. The function of the GHBP has not been defined; however, in vitro studies indicate that it may compete with the GHR for G H binding (5,6). As a potential competitor for ligand binding, the GHBP may have a role distinct from that of the GHR in modulating tissue responses to circulating GH.…”

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confidence: 99%

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Tissue-Specific Developmental Regulation of the Messenger Ribonucleic Acids Encoding the Growth Hormone Receptor and the Growth Hormone Binding Protein in Rat Fetal and Postnatal Tissues

et al. 1992

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ABSTRACT. Tissue responsiveness to growth hormone is likely to be regulated by local concentrations and availability of the membrane-bound growth hormone receptor (GHR) and perhaps by the actions of the soluble growth hormone binding protein (GHBP). To determine whether the developmental regulation of the GHR and GHBP might vary among tissues, we have measured the relative abundance of the 4.3-kb GHR and 1.3-kb GHBP mRNA in rat fetal and postnatal liver, kidney, lung, and ileum by Northern hybridization of polyadenylated RNA with a 32P-labeled antisense riboprobe prepared from a rat GHR cDNA. The GHR and GHBP mRNA were both present in the four tissues studied at fetal age 19 d (E19). In postnatal liver, both transcripts increased in abundance 3-to 4-fold after 14 d to mature levels at 42 d ( p = 0.0001). Similar changes were seen in postnatal kidney for GHR mRNA abundance; however, GHBP mRNA abundance increased only 2-to 3-fold to mature levels by 28 d (kidney GHR versus GHBP mRNA profile, p = 0.0001). In lung, a 2-fold linear increase in GHR mRNA abundance was observed (p = 0.0019), but the GHBP mRNA did not change (GHR versus GHBP mRNA profile, p = 0.0006). Both transcripts decreased in abundance by 2-to 3-fold from E l 9 to 42 d in ileum (p < 0.05). The abundance of both transcripts was three to 10 times greater in 60-d liver than in the other three tissues at 60 d. The variation in abundance and in the developmental profiles of the GHR and GHBP mRNA observed in these fetal and postnatal tissues suggests that the GHR and GHBP could mediate differences within and between tissues in the responsiveness to growth hormone. The differential regulation of the two transcripts evident in kidney and lung supports the emerging evidence that the GHBP may have a function distinct from that of the GHR. (Pediatr Res 31: 335-339, 1992) Abbreviations GH, growth hormone GHR, growth hormone receptor GHBP, growth hormone binding protein poly A+, polyadenylated RNA

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Section: Liver Kidney Ileum Lungmentioning

confidence: 99%

Section: Liver Kidney Ileum Lungmentioning

confidence: 99%

mentioning

confidence: 99%

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Tissue-Specific Developmental Regulation of the Messenger Ribonucleic Acids Encoding the Growth Hormone Receptor and the Growth Hormone Binding Protein in Rat Fetal and Postnatal Tissues

et al. 1992

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“…GHBPs themselves were postulated to cause GH resistance in one GH-resistant cohort (Rieu et al 1993). This hypothesis was based on the ability of recombinant GHBPs to inhibit GH action in vitro by sequestering available GH (Lim et al 1990, Mannor et al 1991. The excess GHBPs in this group may, however, simply reflect a defect outside the GH-binding region that blocks GH action and removes GH-induced GHR/GHBP down-regulation (Merimee et al 1990).…”

Section: Etiologymentioning

confidence: 99%

Growth hormone resistance: clinical states and animal models

Hull¹,

Harvey²

1999

Journal of Endocrinology

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GH exerts pleiotropic effects on growth and metabolism through the GH receptor. A deficiency in the GH receptor gene is thus associated with GH resistance and dwarfism. Complete GH resistance in humans, or Laron syndrome, has been associated with numerous inherited defects in the GH receptor, including point mutations, complete or partial gene deletions, and splice site alterations. Analysis of the GH receptor genes of these patients has provided considerable insight into structure-function relationships of the GH receptor. However, the relative rarity of this disease and the obvious difficulties involved in human research have prompted a search for an animal model of GH resistance. Numerous models have been proposed, including the sex-linked dwarf chicken, the guinea pig, and the Laron mouse. In this review, the characteristics and etiology of Laron syndrome and these animal models will be discussed. The insight provided by these disorders into the roles and mechanism of action of GH will also be reviewed.

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“…O valor do ponto de corte utilizado para interpretar os níveis de nadir de GH tem sofrido várias modificações com o aumento da sensibilidade e da especificidade dos ensaios (9,13,15,23,36). Empregando RIE policlonal, o valor de nadir de GH inferior a 2,0 µg/l era considerado normal (24,26).…”

Section: Critérios De Curaunclassified

Ensaios para a medida de hormônio do crescimento (GH) e IGF-I: aspectos metodológicos e suas implicações no diagnóstico e seguimento da acromegalia

Casagrande

Czepielewski

2007

Arq Bras Endocrinol Metab

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RESUMOA dosagem do GH no soro é essencial para confirmar ou excluir o seu excesso. Na acromegalia, a ausência de critérios clínicos suficientemente sensíveis para monitorizar o sucesso do tratamento faz com que o GH sérico seja o procedimento de escolha e, para isso, é essencial que a sua dosagem seja realizada de forma confiável, capaz de permitir interpretações uniformes. Vários critérios hormonais têm sido propostos para caracterizar remissão da acromegalia, incluindo níveis séricos de GH randômico inferior a 2,5 µg/l, nadir de GH durante o teste de tolerância oral a glicose inferior a 1,0 µg/l e IGF-I normal para sexo e idade. A importância do tratamento adequado consiste na possibilidade de reverter a mortalidade prematura da acromegalia através da diminuição dos níveis de GH para valores menores que 2,5 µg/l. Com o surgimento de ensaios ultra-sensíveis para medida do GH, tornaram-se necessários critérios mais estritos para determinar cura ou remissão da doença. Nesta revisão, descreveremos aqui as modificações decorrentes da evolução dos ensaios, as conseqüências nos resultados de GH e os pontos de corte propostos na literatura para caracterização da atividade e remissão da acromegalia. ABSTRACT Growth Hormone (GH) and IGF-I Assays: Methodological Aspects and its Implications in Acromegaly Diagnosis and Follow-Up.Growth hormone quantification in serum is essential for confirming or ruling out its excess. The absence of clinical criteria sufficiently sensitive to evaluate the treatment success enables GH as the key diagnostic procedure and for that, its measurements must be done in a reliable way and must allow uniform interpretation. Several different biochemical criteria for remission have been suggested in the past, including a random GH measurement less than 2.5 µg/l, mean GH value from a day curve less than 2.5 µg/l, nadir GH value after an oral glucose tolerance test (OGGT) less than 1.0 µg/l and a normal age-related IGF-I level. The importance of adequate treatment is highlighted by data indicating that lowering GH levels to less than 2.5 µg/l reverses the premature mortality of acromegaly. With the advances of ultrasensitive assays for GH measurement, strictest remission criteria to determine remission or cure were necessary. In this review, we describe the changes of assay methodology and its consequences in serum GH results and cut off point values to define activity and remission of acromegaly.

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Plasma Growth hormone (GH)-binding proteins: effect on GH binding to receptors and GH action

Cited by 18 publications

References 5 publications

Tissue-Specific Developmental Regulation of the Messenger Ribonucleic Acids Encoding the Growth Hormone Receptor and the Growth Hormone Binding Protein in Rat Fetal and Postnatal Tissues

Tissue-Specific Developmental Regulation of the Messenger Ribonucleic Acids Encoding the Growth Hormone Receptor and the Growth Hormone Binding Protein in Rat Fetal and Postnatal Tissues

Growth hormone resistance: clinical states and animal models

Ensaios para a medida de hormônio do crescimento (GH) e IGF-I: aspectos metodológicos e suas implicações no diagnóstico e seguimento da acromegalia

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