Growth hormone (GH) status regulates GH receptor and GH binding protein mRNA in a tissue- and transcript-specific manner but has no effect on insulin-like growth factor-I receptor mRNA in the rat

A. A. Butler, B. Funk, B. H. Breier, D. LeRoith, Charles Roberts, P. D. Gluckman

    Research output: Contribution to journalArticle

    22 Citations (Scopus)

    Abstract

    The effect of growth hormone-deficiency (GHD) and treatment with recombinant bovine GH (bGH) or human IGF-I (hIGF-I) for 10 days on the expression of GH receptor (GHR). GH binding protein (GHBP) and of insulin-like growth factor-I receptor (IGF-IR) mRNA was examined using dw/dw and normal Lewis rats. Hepatic GHR and GHBP mRNA expression was significantly lower in dw/dw rats in comparison to Lewis rats (P <0.01) while specific 125I-bGH binding to hepatic microsomal membranes was significantly higher (P <0.01), suggesting a reduction in hepatic GHR turnover with GHD. Treatment with bGH reduced hepatic specific 125I-bGH binding in dw/dw rats, but had no effect in Lewis rats. Treatment with hIGF-I increased hepatic specific 125I-bGH binding in Lewis rats. Hepatic GHR and GHBP mRNA expression was not changed by bGH or hIGF-I treatment, suggesting that differences in hepatic specific 125I-bGH binding may be due to posttranscriptional mechanisms. GHBP mRNA expression was higher in kidney, heart, and muscle of dw/dw rats in comparison to Lewis rats (P <0.01), while GHR mRNA abundance was not changed. Treatment of dw/dw rats with hIGF-I or bGH resulted in a coordinate reduction of GHR and GHBP mRNAs in kidney (P <0.01). IGF-IR mRNA was not detected in liver and despite reduced plasma IGF-I levels and IGF-I mRNA expression IGF-IR mRNA abundance was not changed in nonhepatic tissues by GHD. Our data suggest that changes in plasma IGF-I levels and local IGF-I mRNA do not influence IGF-IR mRNA expression, while GHR and GHBP mRNA expression in different rat tissues are regulated independently. The increased nonhepatic GHBP mRNA expression with GHD suggests that nonhepatic GHBP may have an important physiological function distinct from that of GHBP in liver or in plasma.

    Original languageEnglish (US)
    Pages (from-to)181-189
    Number of pages9
    JournalMolecular and Cellular Endocrinology
    Volume116
    Issue number2
    DOIs
    StatePublished - Feb 5 1996

    Fingerprint

    Somatotropin Receptors
    IGF Type 1 Receptor
    Growth Hormone
    Rats
    Tissue
    Messenger RNA
    Insulin-Like Growth Factor I
    Liver
    Plasmas
    somatotropin-binding protein
    Kidney
    Muscle

    Keywords

    • (GH binding protein)
    • (GH receptor)
    • (IGF-I receptor)
    • GH
    • mRNA
    • Rat

    ASJC Scopus subject areas

    • Endocrinology
    • Endocrinology, Diabetes and Metabolism

    Cite this

    Growth hormone (GH) status regulates GH receptor and GH binding protein mRNA in a tissue- and transcript-specific manner but has no effect on insulin-like growth factor-I receptor mRNA in the rat. / Butler, A. A.; Funk, B.; Breier, B. H.; LeRoith, D.; Roberts, Charles; Gluckman, P. D.

    In: Molecular and Cellular Endocrinology, Vol. 116, No. 2, 05.02.1996, p. 181-189.

    Research output: Contribution to journalArticle

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    abstract = "The effect of growth hormone-deficiency (GHD) and treatment with recombinant bovine GH (bGH) or human IGF-I (hIGF-I) for 10 days on the expression of GH receptor (GHR). GH binding protein (GHBP) and of insulin-like growth factor-I receptor (IGF-IR) mRNA was examined using dw/dw and normal Lewis rats. Hepatic GHR and GHBP mRNA expression was significantly lower in dw/dw rats in comparison to Lewis rats (P <0.01) while specific 125I-bGH binding to hepatic microsomal membranes was significantly higher (P <0.01), suggesting a reduction in hepatic GHR turnover with GHD. Treatment with bGH reduced hepatic specific 125I-bGH binding in dw/dw rats, but had no effect in Lewis rats. Treatment with hIGF-I increased hepatic specific 125I-bGH binding in Lewis rats. Hepatic GHR and GHBP mRNA expression was not changed by bGH or hIGF-I treatment, suggesting that differences in hepatic specific 125I-bGH binding may be due to posttranscriptional mechanisms. GHBP mRNA expression was higher in kidney, heart, and muscle of dw/dw rats in comparison to Lewis rats (P <0.01), while GHR mRNA abundance was not changed. Treatment of dw/dw rats with hIGF-I or bGH resulted in a coordinate reduction of GHR and GHBP mRNAs in kidney (P <0.01). IGF-IR mRNA was not detected in liver and despite reduced plasma IGF-I levels and IGF-I mRNA expression IGF-IR mRNA abundance was not changed in nonhepatic tissues by GHD. Our data suggest that changes in plasma IGF-I levels and local IGF-I mRNA do not influence IGF-IR mRNA expression, while GHR and GHBP mRNA expression in different rat tissues are regulated independently. The increased nonhepatic GHBP mRNA expression with GHD suggests that nonhepatic GHBP may have an important physiological function distinct from that of GHBP in liver or in plasma.",
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