Insulin-like growth factor-binding protein-2 (IGFBP-2) overexpression negatively regulates bone size and mass, but not density, in the absence and presence of growth hormone/IGF-I excess in transgenic mice

2002 ◽  
Vol 206 (1-2) ◽  
pp. 139-148 ◽  
Author(s):  
Felix Eckstein ◽  
Tatjana Pavicic ◽  
Sabine Nedbal ◽  
Corina Schmidt ◽  
Ulrich Wehr ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Growth Factor ◽  
Transgenic Mice ◽  
Binding Protein ◽  
Bone Size ◽  
Insulin Like Growth Factor ◽  
Factor Binding ◽  
Igf I

scholarly journals Growth Inhibition in Giant Growth Hormone Transgenic Mice by Overexpression of Insulin-Like Growth Factor-Binding Protein-2

Endocrinology ◽  
2001 ◽  
Vol 142 (5) ◽  
pp. 1889-1898 ◽  
Author(s):  
Andreas Hoeflich ◽  
Sabine Nedbal ◽  
Werner F. Blum ◽  
Michael Erhard ◽  
Harald Lahm ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Growth Factor ◽  
Transgenic Mice ◽  
Growth Inhibition ◽  
Binding Protein ◽  
Insulin Like Growth Factor ◽  
Factor Binding

A homologous radioimmunoassay for ovine insulin-like growth factor-binding protein-2: ontogenesis and the response to growth hormone, placental lactogen and insulin-like growth factor-I treatment in sheep

1995 ◽  
Vol 144 (1) ◽  
pp. 75-82 ◽  
Author(s):  
B W Gallaher ◽  
B H Breier ◽  
W F Blum ◽  
S N McCutcheon ◽  
P D Gluckman
Keyword(s):  
Growth Hormone ◽  
Growth Factor ◽  
Binding Protein ◽  
Negative Relationship ◽  
Serum Levels ◽  
Treated Group ◽  
Placental Lactogen ◽  
Insulin Like Growth Factor ◽  
Factor Binding ◽  
Igf I

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

Long-term treatment of Laron type dwarfs with insulin-like growth factor-1 increases serum insulin-like growth factor-binding protein-3 in the absence of growth hormone activity

1993 ◽  
Vol 128 (2) ◽  
pp. 144-149 ◽  
Author(s):  
Hannah Kanety ◽  
Avraham Karasik ◽  
Beatrice Klinger ◽  
Aviva Silbergeld ◽  
Zvi Laron
Keyword(s):  
Growth Hormone ◽  
Growth Factor ◽  
Binding Protein ◽  
Serum Insulin ◽  
Continuous Treatment ◽  
Insulin Like Growth Factor ◽  
Factor Binding ◽  
Long Term Treatment ◽  
Igf I ◽  
Igfbp 3

Insulin-like growth factor binding protein-3 (IGFBP-3) is the major carrier of insulin-like growth factor I (IGF-1) in serum, and its production is growth hormone (GH) dependent. It is unclear whether in humans IGFBP-3 production is directly regulated by GH or mediated via IGF-I. We addressed this question in six patients with Laron-type dwarfism, a syndrome characterized by the absence of GH receptor activity (LTD), who were chronically treated with recombinant IGF-I. Analysis of the electrophoretic profiles of serum IGFBPs in these patients by Western ligand blotting revealed an extremely low IGFBP-3 level. A striking progressive increase in serum IGFBP-3 was observed with continuous treatment, despite the absence of GH action. In LTD children, serum IGFBP-3 increased up to 19-fold after six months of therapy and equalled levels observed in controls, whereas in adult LTD patients the increase was smaller. A rise in serum levels of 34, 30 and 24 kDa BPs (presumably IGFBP-2, -1 and -4, respectively was also noted with chronic IGF-I therapy. This proof of GH-independent induction of IGFBP-3 by IGF-1 may be a major advantage in the therapeutic use of biosynthetic IGF-I in several types of short stature children.

Insulin‐like growth factor binding protein 2 (IGFBP‐2) separates hypertrophic and hyperplastic effects of growth hormone (GH)/IGF‐I excess on adrenocortical cells in vivo

2002 ◽  
Vol 16 (13) ◽  
pp. 1721-1731 ◽  
Author(s):  
Andreas Hoeflich ◽  
Matthias M. Weber ◽  
Thomas Fisch ◽  
Sabine Nedbal ◽  
Christian Fottner ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Growth Factor ◽  
Binding Protein ◽  
Insulin Like Growth Factor ◽  
Adrenocortical Cells ◽  
Factor Binding ◽  
Igf I

scholarly journals Impaired adipogenesis in insulin-like growth factor binding protein-1 transgenic mice

1999 ◽  
Vol 162 (3) ◽  
pp. 457-465 ◽  
Author(s):  
K Rajkumar ◽  
T Modric ◽  
LJ Murphy
Keyword(s):  
Growth Factor ◽  
Transgenic Mice ◽  
Binding Protein ◽  
Critical Role ◽  
Insulin Like Growth Factor ◽  
Wild Type ◽  
Factor Binding ◽  
Igf I ◽  
Enhanced Expression ◽  
Glycerol 3 Phosphate Dehydrogenase

Differentiation of precursor cells into mature fat cells is accompanied by enhanced expression of insulin-like growth factor (IGF)-I and is stimulated by multiple hormones including growth hormone, glucocorticoids, IGF-I and insulin. We used transgenic mice that overexpress insulin-like growth factor binding protein-1 to investigate the role of IGF-I in the accumulation of fat tissue. In response to a sucrose-enriched diet, transgenic mice gained significantly less body weight and the epididymal fat mass was significantly reduced compared with wild-type mice. The increase in adipocyte size was also significantly reduced in transgenic mice compared with wild-type mice. Fewer colonies were generated from adipose tissue from transgenic mice and the mitogenic response of these cells to IGF-I was significantly reduced compared with those from wild-type mice. Induction of glycerol-3-phosphate dehydrogenase, a measure of adipocyte differentiation, by IGF-I but not insulin, was reduced in preadipocytes from transgenic mice. These data indicate that IGF-I has a critical role in the proliferation of adipocyte precursors, the differentiation of preadipocytes and the development of obesity in response to calorie excess.

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