Normal somatomedin-C/insulin-like growth factor I binding and action in cultured human fibroblasts from Turner syndrome

1983 ◽  
Vol 104 (4) ◽  
pp. 502-509 ◽  
Author(s):  
Ron G. Rosenfeld ◽  
Laura A. Dollar ◽  
Raymond L. Hintz ◽  
Cheryl Conover
Keyword(s):  
Growth Factor ◽  
Turner Syndrome ◽  
Thymidine Incorporation ◽  
Insulin Like Growth Factor ◽  
Cell Replication ◽  
Somatomedin C ◽  
Factor I ◽  
Igf I ◽  
And Control ◽  
Stimulation Of

Abstract. Growth retardation is a major manifestation of Turner syndrome (TS). Since plasma growth hormone and somatomedin-C/insulin-like growth factor I (SM-C/IGF-I) levels are generally normal, growth failure has been ascribed to peripheral defects in SM-C/IGF-I receptors or action. We have measured the binding of [125I]SM-C/IGF-I to cultured fibroblast monolayers derived from patients with Turner syndrome, and have evaluated SM-C/IGF-I stimulation of both [3H]thymidine incorporation and cell replication. When compared to fibroblasts from normal adults, newborns, and agematched children, no significant differences were observed in specific binding of [125I]SM-C/IGF-I to fibroblast monolayers, and displacement curves demonstrated similar receptor affinities for all groups. Similarly, equivalent SM-C/IGF-I stimulation of [3H]thymidine incorporation was seen in both Turner and control fibroblasts. In the absence of serum, SM-C/IGF-I, at a concentration of 10–25 ng/ml, stimulated thymidine incorporation 3.7–11.8-fold in Turner fibroblasts and 1.9–9.8-fold in control cells. In combination with 1.0% human hypopituitary serum (HHS), SM-C/IGF-I stimulated thymidine incorporation 20–70-fold in all cell lines. Cell replication in both TS and control cells was increased 90% by the combination of SM-C/IGF-I + 0.5% HHS, and 140% by SM-C/IGF-I + 0.5% HHS + dexamethasone. We conclude that TS fibroblasts have normal SM-C/IGF-I receptors and sensitivity, and are capable of enhanced DNA synthesis and replication following SM-C/IGF-I stimulation.

INSULIN-LIKE GROWTH FACTOR I/SOMATOMEDIN C (IGF-I/Sm C): COMPARISON OF NATURAL, SOLID PHASE SYNTHETIC AND RECOMBINANT DNA ANALOG PEPTIDES IN TWO RADIOLIGAND ASSAYS

Endocrinology ◽  
1984 ◽  
Vol 115 (6) ◽  
pp. 2490-2492 ◽  
Author(s):  
DON SCHALCH ◽  
DORIS REISMANN ◽  
CAROL EMLER ◽  
RENE HUMBEL ◽  
CHOH HAO LI ◽  
...  
Keyword(s):  
Growth Factor ◽  
Recombinant Dna ◽  
Solid Phase ◽  
Insulin Like Growth Factor ◽  
Somatomedin C ◽  
Factor I ◽  
Igf I ◽  
Growth Factor I

scholarly journals Circulating Forms of Insulin-like Growth Factor-I (IGF-I) /Somatomedin C (SMC) in Fetal Life

1989 ◽  
Vol 65 (3) ◽  
pp. 137-151
Author(s):  
Atsuko YAMASAKI ◽  
Hajime MORIKAWA ◽  
Yasuo UEDA ◽  
Matsuto MOCHIZUKI
Keyword(s):  
Growth Factor ◽  
Fetal Life ◽  
Insulin Like Growth Factor ◽  
Somatomedin C ◽  
Factor I ◽  
Igf I ◽  
Growth Factor I

Insulin and growth hormone act synergistically to stimulate insulin-like growth factor-I production by cultured chicken hepatocytes

1991 ◽  
Vol 128 (3) ◽  
pp. 389-393 ◽  
Author(s):  
B. Houston ◽  
I. E. O'Neill
Keyword(s):  
Growth Factor ◽  
Insulin Like Growth Factor ◽  
Free Medium ◽  
In Vitro System ◽  
Factor I ◽  
Maximal Stimulation ◽  
Igf I ◽  
Growth Factor I ◽  
Stimulation Of

ABSTRACT Cultured chicken hepatocytes were used to investigate whether insulin and GH interact to regulate insulin-like growth factor-I (IGF-I) production in vitro. In the first set of experiments hepatocytes were preincubated for 6 h in hormone-free medium, and the effects of various combinations of insulin and GH on IGF-I production over the next 24 h were quantified by radioimmunoassay. Basal IGF-I production was 5·36 pg IGF-I/μg DNA and this was increased 1·31±0·13-fold (mean ± s.e.m.) by insulin, 1·90±0·24-fold by GH and 4·46±0·68-fold by a combination of insulin and GH. These results demonstrate that insulin and GH interact synergistically to stimulate IGF-I production in vitro. The synergism with GH occurred at physiological concentrations of insulin with half-maximal stimulation occurring at an insulin concentration of 6 ng/ml. In hepatocytes which had been exposed to insulin immediately before the start of the experiment, the presence of insulin was no longer required for maximal stimulation of IGF-I production by GH. This in-vitro system will facilitate the study of the molecular basis of the interaction between insulin and GH. Journal of Endocrinology (1991) 128, 389–393

Recombinant growth hormone and insulin-like growth factor I do not alter gonadotrophin stimulation of the baboon testis in vivo

1994 ◽  
Vol 131 (4) ◽  
pp. 405-412 ◽  
Author(s):  
Bronwyn A Crawford ◽  
David J Handelsman
Keyword(s):  
Growth Hormone ◽  
Growth Factor ◽  
Insulin Like Growth Factor ◽  
Recombinant Growth Hormone ◽  
Factor I ◽  
Igf I ◽  
Growth Factor I ◽  
Human Primate ◽  
Stimulation Of

Crawford BA, Handelsman DJ. Recombinant growth hormone and insulin-like growth factor I do not alter gonadotrophin stimulation of the baboon testis in vivo. Eur J Endocrinol 1994;131:405–12. ISSN 0804–4643 In vitro studies indicate a physiological role for insulin-like growth factor I (IGF-I) in paracrine regulation of testicular function and recent clinical studies suggest a potential role for growth hormone (GH) and/or IGF-I in the treatment of hypogonadotrophic states in males. This study aimed to examine the effects of pretreatment with recombinant human GH (rhGH) or rhIGF-I on the response to gonadotrophins of the non-human primate testis in vivo. Using a balanced Latin square design with repeated measures, six prepubertal male hamadryas baboons (Papio hamadryas hamadryas) were treated in a cross-over sequence for periods of 18 days with daily im injections of rhGH (0.4 IU·kg−1 · day−1), rhIGF-I (0.1 mg·kg−1 · day−1) or saline with a 2-week washout period between each treatment. A single im injection of hCG (1500 IU) increased serum testosterone (p = 0.0002) but neither rhGH nor rhIGF-I influenced the timing or magnitude of this response (p > 0.5). A single im dose of FSH (75 IU) stimulated immunoreactive inhibin (p = 0.01) but also was unaffected in magnitude or timing by pretreatment with rhGH or rhIGF-I (p> 0.2). Circulating IGF-I levels were increased independently by hCG (p = 0.01) and FSH (p < 0.0001) administration. These findings indicate that neither GH nor IGF-I pre-treatment enhance acute gonadal responses to gonadotrophin stimulation of the prepubertal non-human primate testis in vivo. These findings suggest that GH or IGF-I treatment of hypogonadotrophic men without somatotrophin deficiency is unlikely to be beneficial. David J Handelsman, Andrology Unit, Royal Prince Alfred Hospital, Departments of Medicine and Obstetrics and Gynaecology, University of Sydney, Sydney 2006, Australia

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