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  • 1
    Electronic Resource
    Electronic Resource
    Plasma Growth hormone (GH)-binding proteins: effect on GH binding to receptors and GH action (1992)
    Springer
    Pediatric nephrology 6 (1992), S. 272-272 
    Details
    ISSN: 1432-198X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00878369
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    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Growth hormone binding protein and free growth hormone in chronic renal failure (1996)
    Springer
    Pediatric nephrology 10 (1996), S. 328-330 
    Details
    ISSN: 1432-198X
    Keywords: Growth hormone receptor ; Growth hormone binding protein ; Growth hormone insensitivity ; Chronic renal failure ; Growth failure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Chronic renal failure in children is associated with growth failure. While the pathogenesis of uremic growth failure is multifactorial, an abnormal growth hormone/insulin-like growth factor (GH-IGF) axis is an important contributory element. Patients with uremia exhibit insensivivity to the action of GH, as exemplified by high plasma GH levels, low IGF-I activity, and poor somatic growth. This insensitivity can be overcome by supraphysiological doses of exogenous GH. Plasma GH binding protein (GHBP, the circulating ectodomain of the GH receptor) levels are decreased in patients with renal failure, as are hepatic GH receptor levels in animal models. Since GHBP levels are thought to reflect GH receptor levels in tissues, it is likely that the uremic GH insensitivity in humans is mediated by a decreased number of GH receptors. Another implication of the low plasma GHBP is a disproportionate elevation of free plasma GH (the biologically active moiety) relative to total GH, lending additional support to the concept of GH insensitivity in uremia. GH kinetics are altered in renal failure because of: (1) inability to excrete GH and (2) changes in the bound fraction of GH in the circulation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00866772
    Location Call Number Limitation Availability
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    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Growth hormone binding protein and free growth hormone in chronic renal failure (1996)
    Springer
    Pediatric nephrology 10 (1996), S. 328-330 
    Details
    ISSN: 1432-198X
    Keywords: Key words: Growth hormone receptor   ;   Growth hormone binding protein   ;   Growth hormone insensitivity   ;   Chronic renal failure   ;   Growth failure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Chronic renal failure in children is associated with growth failure. While the pathogenesis of uremic growth failure is multifactorial, an abnormal growth hormone / insulin-like growth factor (GH-IGF) axis is an important contributory element. Patients with uremia exhibit insensitivity to the action of GH, as exemplified by high plasma GH levels, low IGF-I activity, and poor somatic growth. This insensitivity can be overcome by supraphysiological doses of exogenous GH. Plasma GH binding protein (GHBP, the circulating ectodomain of the GH receptor) levels are decreased in patients with renal failure, as are hepatic GH receptor levels in animal models. Since GHBP levels are thought to reflect GH receptor levels in tissues, it is likely that the uremic GH insensitivity in humans is mediated by a decreased number of GH receptors. Another implication of the low plasma GHBP is a disproportionate elevation of free plasma GH (the biologically active moiety) relative to total GH, lending additional support to the concept of GH insensitivity in uremia. GH kinetics are altered in renal failure because of: (1) inability to excrete GH and (2) changes in the bound fraction of GH in the circulation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00866772
    Location Call Number Limitation Availability
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    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    The orientation of insulin receptors in the red cell membrane (1983)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 21 (1983), S. 233-237 
    Details
    ISSN: 0730-2312
    Keywords: insulin receptors ; receptor asymmetry ; inverted membrane vesicles ; red cell membrane ; cytoplasmic membrane surface ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: High-affinity binding of insulin to receptors in human erythrocyte membranes occurred at the external surface, but not at the cytoplasmic surface of the plasma membrane, as assessed by insulin binding to right-side-out and inside-out membrane vesicles. Even after prolonged (3 h) incubation at 22°C, binding at the cytoplasmic membrane aspect remained negligible. The data indicate that the insulin receptor displays its hormone-binding site exclusively toward the extracellular space and that transmembrane mobility (“flip-flop”) of the receptor from one to the other membrane leaflet is severely restricted.
    Additional Material: 1 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240210305
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    Paper (German National Licenses)
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