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Growth hormone treatment in children with preterminal chronic renal failure: No adverse effect on glomerular filtration rate (1992)

Tönshoff, B. ; Tönshoff, C. ; Mehls, O. ; [et al.]

Springer

European journal of pediatrics 151 (1992), S. 601-607

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ISSN: 1432-1076

Keywords: Chronic renal failure ; Recombinant human growth hormone treatment ; Insulin-like growth factors ; Insulin-like growth factor binding proteins ; Progression of renal disease

Source: Springer Online Journal Archives 1860-2000

Topics: Medicine

Notes: Abstract Impaired growth and stunting remains a major therapeutic problem in children with chronic renal failure (CRF). Recombinant human growth hormone (rhGH) treatment may be beneficial, but concern has been raised about possible side-effects, i.e. deterioration of renal function and glucose intolerance. We have treated 10 prepubertal children with CRF (median age 7.5 [1.7–10.0] years) with 4 IU rhGH/m2 per day s.c. over a period of 1 year. Height velocity increased significantly (P〈0.03) from basal 4.6 (2.0–14.0) cm/year to 9.7 (6.8–17.6) cm/year. Height velocity SDS for chronological age and for bone age increased in all children from basal median −2.3 to +3.8 (P〈0.005). Median glomerular filtration rate (GFR) measured by single injection inulin clearance at onset was 18 (11–66) ml/min per 1.73 m2 and did not change significantly during the treatment year. The loss of GFR as estimated by creatinine clearance was similar during the treatment year (median loss 1.3 ml/min per 1.73 m2) compared to the year before treatment (median loss 3.7 ml/min per 1.73 m2). Serum glucose levels during an oral glucose tolerance test did not change, but fasting as well as stimulated insulin levels increased significantly with time during the study period. It is concluded that the rhGH regimen employed was remarkably effective in improving growth velocity in children with CRF without adversely affecting GFR. Glucose homeostasis remained stable, but at the expense of increased serum insulin levels.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1007/BF01957731

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Human osteosarcoma (U-2 OS) cells express both insulin-like growth factor-I (IGF-I) receptors and insulin-like growth factor-II/mannose-6-phosphate (IGF-II/M6P) receptors and synthesize IGF-II: Autocrine growth stimulation by IGF-II via the IGF-I receptor (1994)

Raile, K. ; Höflich, A. ; Kessler, U. ; [et al.]

New York, NY [u.a.] : Wiley-Blackwell

Journal of Cellular Physiology 159 (1994), S. 531-541

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ISSN: 0021-9541

Keywords: Life and Medical Sciences ; Cell & Developmental Biology

Source: Wiley InterScience Backfile Collection 1832-2000

Topics: Biology , Medicine

Notes: Recently, insulin-like growth factor-I and -II (IGF-I and -II) have been implicated in the growth promotion of tumors in vivo and tumor cells in vitro. We have studied the human osteosarcoma cell line U-2 OS in order (1) to gain more insight into the growth promoting actions of the IGFs and (2) to establish an in vitro tissue culture model of IGF action in human tumor cells. Specific binding of 125I-IGF-I and 125I-IGF-II to IGF-I receptors and IGF-II/mannose-6-phosphate (M6P) receptors on U-2 OS cells was demonstrated in competitive binding experiments and in affinity crosslinking experiments. Western blotting of cell extracts confirmed the expression of the IGF-II/M6P receptor. In addition, in Northern blotting experiments using total RNA from U-2 OS cells IGF-I receptor RNA of 11 kb and IGF-II/M6P receptor RNA of approximately 9 kb were detected. Solution hybridization experiments confirmed the presence of IGF-I receptor and IGF-II/M6P receptor RNA. In a subset of experiments DNA synthesis was measured as 3H-thymidine uptake into cellular DNA of U-2 OS cells. Normal rat serum stimulated DNA synthesis maximally. IGF-I-deficient serum from hypophysectomized rats as well as IGF-I or IGF-II without serum were approximately twofold and tenfold, respectively, less potent than serum in stimulating 3H-thymidine uptake. The concentrations of IGF-I and IGF-II needed for half maximal stimulation of DNA synthesis corresponded well with the respective concentrations required for half maximal inhibition of 125I-IGF-I binding to U-2 OS cells. The anti-IGF-I receptor antibody alphaIR3 blocked the IGF-I and IGF-II stimulated increase of 3H-thymidine uptake. In addition, basal DNA synthesis was partially inhibited by the anti-IGF-I receptor antibody. These data suggest that U-2 OS cells synthesize and secrete IGF-like peptides. Northern blotting experiments confirmed that U-2 OS cells express an IGF-II RNA species of 5.3 kb but no IGF-I transcripts. In a series of RNase protection assays, protected RNA fragments were detected with an IGF-II riboprobe. © 1994 wiley-Liss, Inc.

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