scholarly journals Effects of Insulin on Serum Levels of Growth Hormone (GH), Insulin-like Growth Factor (IGF)-I and IGF-I Binding Activity in Chickens.

1998 ◽  
Vol 35 (4) ◽  
pp. 256-259
Author(s):  
Masaaki WAKITA ◽  
Mayumi KATAOKA ◽  
Sadao HOSHINO
1995 ◽  
Vol 144 (1) ◽  
pp. 75-82 ◽  
Author(s):  
B W Gallaher ◽  
B H Breier ◽  
W F Blum ◽  
S N McCutcheon ◽  
P D Gluckman

Abstract Although insulin-like growth factor-binding protein-2 (IGFBP-2) is an abundant IGFBP in fetal and postnatal plasma, its regulation is not yet clearly understood. To address this question in sheep, we purified ovine IGFBP-2 and developed a homologous radioimmunoassay. We have studied its ontogenesis and measured serum concentrations of ovine IGFBP-2 after bovine growth hormone (bGH), ovine placental lactogen (oPL) and IGF-I treatment. Concentrations of IGFBP-2 were high at 125 days of gestation (550 ± 15 μg/l) but fell after birth P<0·05) and plateaued after 1 year of age (340 ± 20 μg/l). In lactating ewes, bGH treatment for 7 days significantly reduced (21%; P<0·05) IGFBP-2 relative to the saline-treated group. Similarly, in neonatal lambs, bGH treatment from day 3 to day 23 of life reduced (P<0·05) IGFBP-2 by 23% relative to the saline-treated group. oPL had no effect on serum levels of IGFBP-2 in the ewe or the neonatal lamb. In well-fed yearling lambs, treatment with IGF-I reduced IGFBP-2 values by 27% (P<0·05) relative to control animals. In yearling lambs, reduced nutrition increased plasma IGFBP-2 (41%; P<0·05). However this increase was abolished by IGF-I treatment. The changes in plasma levels of IGFBP-2 were positively related to changes in IGF-II while there was a negative relationship between circulating IGF-I and IGFBP-2 such that both IGF-I and IGF-II may play a role in the regulation of IGFBP-2 in serum. Journal of Endocrinology (1995) 144, 75–82


1994 ◽  
Vol 131 (2) ◽  
pp. 150-155 ◽  
Author(s):  
M Kassem ◽  
K Brixen ◽  
W Blum ◽  
L Mosekilde ◽  
EF Eriksen

Kassem M, Brixen K, Blum W, Mosekilde L, Eriksen EF. No evidence for reduced spontaneous or growth-hormone-stimulated serum levels of insulin-like growth factor (IGF)-I, IGF-II or IGF binding protein 3 in women with spinal osteoporosis. Eur J Endocrinol 1994;131:150–5. ISSN 0804–4643 To test the hypothesis that a dysfunctional growth hormone (GH)–insulin-like growth factor (IGF) axis may play a role in the pathogenesis of osteoporosis, we compared the levels of IGF-I, IGF-II and IGF binding protein 3 (IGFBP-3) in 15 women with spinal osteoporosis (i.e. at least one non-traumatic vertebral fracture) and 15 normal age-matched women. Furthermore, the response to 3 days' treatment with recombinant human GH (r-hGH) (0.2 IU kg−1·day−1) was determined. The basal levels of IGF-I, IGF-II and IGFBP-3 were similar in patients and controls (mean ± sem): IGF-I, 16.5 ± 1.3 versus 16.0 ± 1.3 nmol/l (NS); IGF-II, 79.9 ± 3.6 versus 72.5 ± 4.1 nmol/l (NS); and IGFBP-3, 125.7 ± 6.5 versus 130.3 ± 7.8 nmol/l (NS). Stimulation with r-hGH elicited increased levels of IGF-I, IGF-II and IGFBP-3 within both groups (p < 0.001). The maximal values expressed as a percentage of baseline were: IGF-I, 341 ± 26% versus 369 ± 22%, IGF-II, 125 ± 4% versus 119 ± 5%, IGFBP-3, 141 ± 5% versus 147 ± 7% in osteoporotic patients and controls, respectively. No significant differences were observed between patients and controls in either their maximal response or in the area under the response curves. Our results do not support the hypothesis of a dysfunctional GH–IGF axis in women with spinal osteoporosis. Kim Brixen, University Department of Endocrinology and Metabolism, Aarhus Amtssygehus, Tage-Hansens gade 2, DK-8000 Aarhus C, Denmark


1996 ◽  
Vol 271 (2) ◽  
pp. E223-E231 ◽  
Author(s):  
L. Goya ◽  
F. Rivero ◽  
M. A. Martin ◽  
R. Arahuetes ◽  
E. R. Hernandez ◽  
...  

The effect of refeeding and insulin treatment of undernourished and diabetic neonatal rats, respectively, on the regulation of insulin-like growth factor (IGF) and insulin-like growth factor binding protein (IGFBP) was investigated. The changes in body weight, insulinemia, glycemia, serum IGF-I, and growth hormone (GH) as well as the increase of the 30-kDa IGFBP in undernourished and diabetic neonatal rats previously shown elsewhere were reversed by refeeding and insulin treatment, respectively. Also, changes in liver mRNA expression of IGF-I and-II and IGFBP-1 and -2 were restored in refed undernourished and IGF-I and IGFBP-1 levels recovered in insulin-treated diabetic rats. However, serum GH was still below normal after rehabilitation in both situations. Thus the present results support the idea of a GH-independent IGF/ IGFBP regulation mediated by a balance of insulin and nutrients as has already been suggested in previous neonatal studies.


1991 ◽  
Vol 124 (5) ◽  
pp. 602-607 ◽  
Author(s):  
Ben A. A. Scheven ◽  
Nicola J. Hamilton

Abstract. Longitudinal growth was studied using an in vitro model system of intact rat long bones. Metatarsal bones from 18- and 19-day-old rat fetuses, entirely (18 days) or mainly (19 days) composed of chondrocytes, showed a steady rate of growth and radiolabelled thymidine incorporation for at least 7 days in serum-free media. Addition of recombinant human insulin-like growth factor-I to the culture media resulted in a direct stimulation of the longitudinal growth. Recombinant human growth hormone was also able to stimulate bone growth, although this was generally accomplished after a time lag of more than 2 days. A monoclonal antibody to IGF-I abolished both the IGF-I and GH-stimulated growth. However, the antibody had no effect on the growth of the bone explants in control, serum-free medium. Unlike the fetal long bones, bones from 2-day-old neonatal rats were arrested in their growth after 1-2 days in vitro. The neonatal bones responded to IGF-I and GH in a similar fashion as the fetal bones. Thus in this study in vitro evidence of a direct effect of GH on long bone growth via stimulating local production of IGF by the growth plate chondrocytes is presented. Furthermore, endogenous growth factors, others than IGFs, appear to play a crucial role in the regulation of fetal long bone growth.


Sign in / Sign up

Export Citation Format

Share Document