The Acid-Labile Subunit of Human Ternary Insulin-Like Growth Factor-Binding Protein Complex in Girls with Central Precocious Puberty before and during Gonadotropin-Releasing Hormone Analog Therapy

Cisternino, Mariangela; Draghi, M; Lauriola, Silvana; Scarcella, D.; Bernasconi, Sergio; Luca, Filippo De; Lomeo, Angelo; Tatò, Luciano

doi:10.1210/jc.2002-020308

Cited by 12 publications

(10 citation statements)

References 29 publications

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“…Treatment of CPP with gonadotropin-releasing hormone analogs (GnRHa) stops pubertal development and slows growth velocity. In some studies, GH secretion was found to decrease with the decline of gonadal steroids (1,(3)(4)(5). Recently, the reduction of the IGF-I ternary complex formation was attributed to a reduction of ALS (acid-labile subunit of human ternary insulin like the growth factor-binding protein complex), whereas there was no change in IGF-I and IGF-binding protein (IGFBP)-3 levels (4).…”

Section: Introductionmentioning

confidence: 99%

Circulating ghrelin levels in girls with central precocious puberty are reduced during treatment with LHRH analog

Maffeis

Franceschi²,

Moghetti³

et al. 2007

eur j endocrinol

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Decreased levels of ghrelin have been measured in growing children during puberty. No data are available for girls with central precocious puberty (CPP). Aims: To explore ghrelin changes before, during, and after GnRH analog treatment in girls with CPP. Subjects and methods: A sample of 20 Caucasian girls (8.08G0.65 years of age) with CPP was recruited. Height and weight, bone age, LH, FSH, 17b estradiol (E 2 ), and ghrelin were measured before starting treatment with GnRH analog, 18 months after therapy began and again 6 months after therapy discontinuation. Results: LH and E 2 serum levels decreased significantly during treatment (2.45G2.03 vs 0.67G 0.49 UI/l, P!0.01 and 28.17G9.7 vs 15 pmol/l, P!0.01 respectively), returning to baseline levels after the discontinuation of therapy (4.75G1.66 UI/l and 29.23G6.99 pmol/l respectively). LH peaked following LHRH stimulation significantly (P!0.01) decreased during treatment (24.45G 14.17 vs 1.3G0.18 UI/l) and then increased after therapy discontinuation (12.58G6.09, P!0.01). Ghrelin decreased significantly (P!0.05) during treatment (1849G322 vs 1207G637 pg/ml), and increased, though not significantly (PZ0.09) after therapy withdrawal (1567G629 pg/ml). Conclusions:Contrary to what is expected in physiologic puberty, where ghrelin is progressively reduced, the prepubertal hormone milieau induced by GnRHa treatment in patients suffering from central precocious puberty (CPP) did not promote an increase in ghrelin circulating levels. Therefore, in CPP, ghrelin secretion seems to be independent from pubertal development per se. Concomitant estrogen suppression during treatment may play a potential role in the regulation of ghrelin secretion in these girls. European Journal of Endocrinology 156 99-103

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Section: Introductionmentioning

confidence: 99%

Circulating ghrelin levels in girls with central precocious puberty are reduced during treatment with LHRH analog

Maffeis

Franceschi²,

Moghetti³

et al. 2007

eur j endocrinol

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“…RT-PCR assays indicate that IGFALS is expressed ubiquitously in pigs and transcripts are particularly abundant in the liver, lung, white adipose tissue, prostate, epididymis, thyroid and bladder. of IGFALS in serum (Cisternino et al 2002). The dysfunction of IGFALS has been implicated in a subtle impairment of linear growth, a delay in the onset and slow progress of puberty in a 17-year-old boy (Domene et al 2004).…”

Section: Discussionmentioning

confidence: 99%

“…Several studies have demonstrated the important role of IGFALS in growth and development in mammals. For instance, girls with central precocious puberty, who are characterized for enhanced growth velocity and early puberty, have an increased level of IGFALS in serum (Cisternino et al. 2002).…”

Section: Introductionmentioning

confidence: 99%

Characterization of the porcine insulin‐like growth factor‐binding protein, acid‐labile subunit gene: full‐length cDNA and DNA sequence, polymorphisms and expression profile

Ren

Huang

2007

J Animal Breeding Genetics

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Insulin-like growth factor-binding protein acid-labile subunit (IGFALS) is an important glycoprotein in the circulation complex for insulin-like growth factors-I and -II (IGFs). So far only a partial porcine IGFALS sequence is available. We herein report the isolation, characterization, polymorphism identification and expression analysis of the porcine IGFALS gene. A 2000-bp full-length cDNA sequence was determined with 5'- and 3'-Rapid Amplification of cDNA End (RACE) assay. It contains a 1821-bp open reading frame encoding a protein of 606 amino acids with a calculated molecular mass of 66 kDa and a theoretical isoelectric point of 6.89. The deduced IGFALS protein shares high identity (70-80%) with other mammalian IGFALS. We also obtained a full-length genomic DNA sequence of the gene. Similar to the other mammalian orthologues, particularly in terms of exon size and exon/intron boundaries, the porcine IGFALS gene spans a transcription unit of 2990 bp, consisting of two exons and one intron. Three single nucleotide polymorphisms (synonymous mutations) were identified in the DNA sequence. RT-PCR assays indicate that IGFALS is expressed ubiquitously in pigs and transcripts are particularly abundant in the liver, lung, white adipose tissue, prostate, epididymis, thyroid and bladder.

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“…8,9 Although the mechanisms underlying growth deceleration during GnRHa therapy are not completely understood, studies have demonstrated that it is not caused by changes to the growth hormone (GH)-insulin-like growth factor (IGF)-1 axis. [10][11][12][13][14][15][16][17][18] Recent studies have shown that the addition of GH to GnRHa increases the growth velocity and improves the final height in children with CPP as compared with GnRHa treatment alone. 9,12,15 It is suggested that the growth-promoting action of GH in CPP is, in part, somatotropic independent and may occur locally at the growth plate either directly or in cooperation with other growth factors.…”

Section: Introductionmentioning

confidence: 99%

Epidermal growth factor receptor signalling mediates growth hormone-induced growth of chondrocytes from sex hormone-inhibited adolescent rats

Pan

et al. 2011

Clinical and Experimental Pharmacology and Physiology

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1. Growth hormone (GH) has been demonstrated to overcome the inappropriate deceleration of growth rate in children with central precocious puberty treated with gonadotropin-releasing hormone analogue (GnRHa). However, the underlying mechanisms remain largely unclear. In the present study, we investigated the potential involvement of the epidermal growth factor receptor (EGFR) pathway in the growth promotion by GH using in vitro cultured growth plate chondrocytes isolated from adolescent rats treated with GnRHa. 2. Chondrocytes were stimulated with GH in the presence or absence of the Janus tyrosine kinase (JAK) 2 inhibitor AG490 (1, 10 and 100 nmol/L), the EGFR kinase inhibitor AG1478 (0.1, 1 and 10 nmol/L), U0126 (an inhibitor of extracellular signal-regulated kinase (Erk) activation; 10 μmol/L) or a neutralizing antibody against epidermal growth factor (EGF Ab; 0.1, 1 and 10 μg/mL). The proliferation of chondrocytes was assessed by the 3-(4,5-dimethyl-2 thiazoyl)-2,5-diphenyl-2H-tetrazolium bromide assay and immunostaining for proliferating cell nuclear antigen (PCNA). Phosphorylation of Erk1/2 and EGFR was detected by western-blotting. Intracellular mRNA and extracellular protein levels of EGF were detected using reverse transcription-polymerase chain reaction and ELISA, respectively. 3. Growth hormone promoted the proliferation of chondrocytes, which was correlated with increased phosphorylation of Erk1/2 and EGFR and enhanced expression of EGF. Pretreatment with AG490, AG1478, U0126 or EGF Ab completely or partially inhibited the proliferation of chondrocytes and activation of Erk1/2 and EGFR. Pretreatment with AG490, AG1478, or U0126 partially inhibited the expression of EGF. 4. The findings indicate that GH promotes chondrocyte proliferation by activating EGFR signalling.

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The Acid-Labile Subunit of Human Ternary Insulin-Like Growth Factor-Binding Protein Complex in Girls with Central Precocious Puberty before and during Gonadotropin-Releasing Hormone Analog Therapy

Cited by 12 publications

References 29 publications

Circulating ghrelin levels in girls with central precocious puberty are reduced during treatment with LHRH analog

Circulating ghrelin levels in girls with central precocious puberty are reduced during treatment with LHRH analog

Characterization of the porcine insulin‐like growth factor‐binding protein, acid‐labile subunit gene: full‐length cDNA and DNA sequence, polymorphisms and expression profile

Epidermal growth factor receptor signalling mediates growth hormone-induced growth of chondrocytes from sex hormone-inhibited adolescent rats

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