IGFBP mRNA expression in small intestine of  rat during postnatal development

In contrast to the adult gut, the immature intestine is refractory to subcutaneously infused insulin-like growth factor I (IGF-I). IGF binding protein (IGFBP) mRNA expression was characterized in intestinal tissues from 6-, 19-, and 90-day-old rats to determine if changes in local expression could account for this age-related change in IGF-I potency. For all age groups, IGFBP-3 to -6, but not IGFBP-1 or -2, were detected by Northern blot analysis. IGFBP-3, -4, and -5 were more intensely expressed in the 6-day-old rat intestine compared with weanling or adult tissue. In contrast, IGFBP-6 expression peaked at the time of weaning. In situ hybridization showed IGFBP-3 to -6 expression was confined to cells of the lamina propria and submucosa and also in the muscularis layer for IGFBP-5. Furthermore, the pattern of IGFBP-5 localization in the intestine changed with development. The findings indicate that the expression of IGFBP-3 to -6 is higher in the immature intestine compared with the adult intestine, suggesting locally produced IGFBPs may inhibit systemically derived IGF-I action in the intestine. Therefore, changes to local IGFBP expression may contribute to the varying response of the rat intestine to IGF-I peptides during postnatal development.

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Interactions between the ovary and the local IGF-I axis modulate mammary development in prepubertal heifers

Journal of Endocrinology ◽

10.1677/joe.0.1770295 ◽

2003 ◽

Vol 177 (2) ◽

pp. 295-304 ◽

Cited By ~ 22

Author(s):

SD Berry ◽

RD Howard ◽

PM Jobst ◽

H Jiang ◽

RM Akers

Keyword(s):

Mrna Expression ◽

Specific Binding ◽

Mammary Development ◽

Serum Concentrations ◽

Fat Pad ◽

Igf I ◽

Igf Binding ◽

Igf Binding Protein ◽

Local Expression ◽

Igfbp 3

The objective was to determine the effects of ovariectomy and epithelial-stromal interactions on mammary development and local expression of IGF-I and IGF-binding protein (IGFBP) mRNA in prepubertal heifers. An epithelium-free ('cleared') fat pad (CFP) was prepared in two glands in each of 14 Holstein heifers, aged 1-3 Months. Eight of the calves were also ovariectomized. Serum concentrations of GH, IGF-I and prolactin were not affected by ovariectomy. At 6 Months of age, calves were killed to provide mammary samples of parenchyma, CFP and intact fat pad (MFP). Total mammary mass was reduced in ovariectomized calves (130+/-21 g vs 304+/- 25 g; P<0.001), and in several cases parenchymal tIssue was essentially absent. Uterus weight was also reduced by ovariectomy (14.5+/-3.8 g vs 30.4+/-4.5 g; P<0.05). In support of our hypothesis that local IGF-I mediates prepubertal mammary development, mRNA expression of IGF-I was lower in ovariectomized than in control calves (62.1+/-7.8 vs 91.6+/-7.8 arbitrary units; P<0.05). Specific binding of IGF-I to mammary parenchymal microsomes was also reduced by ovariectomy (377+/-142 vs 868+/-82 c.p.m.; P<0.01), suggesting decreased sensitivity to IGF-I. Expression of IGFBP-3 and IGFBP-5 mRNA were not influenced by ovariectomy. Expression of IGF-I, IGFBP-3 and IGFBP-5 mRNA did not differ between CFP and MFP, suggesting that expression of these factors was not influenced by interactions between stroma and developing epithelium. Overall, the data suggested that interactions between the ovary and the local IGF-I axis act to optimize the availability and effectiveness of IGF-I within the gland to stimulate mammary growth.

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IGF-I and IGF-binding protein-3 in plasma of GH-deficient rats

Journal of Endocrinology ◽

10.1677/joe.0.1500067 ◽

1996 ◽

Vol 150 (1) ◽

pp. 67-76 ◽

Cited By ~ 5

Author(s):

A A Butler ◽

B W Gallaher ◽

G R Ambler ◽

P D Gluckman ◽

B H Breier

Keyword(s):

Mrna Expression ◽

Ternary Complex ◽

Insulin Treatment ◽

Binding Protein ◽

Saline Control ◽

Treatment Groups ◽

Igf I ◽

Igf Binding ◽

Igf Binding Protein ◽

Igfbp 3

Abstract The majority of IGF-I circulates in a large (150 kDa) ternary complex with IGF-binding protein-3 (IGFBP-3) and a non-IGF-binding acid-labile subunit. The secretion of ternary complex into the circulation from liver has been considered to be GH-dependent; however, recent data indicate that GH does not directly regulate hepatic IGFBP-3 synthesis. To examine the role of insulin in regulating plasma IGFBP-3 levels, postpubertal male GH-deficient (dw/dw) rats were treated every 8 h with injections (s.c.) of 0·9% saline, 20 μg insulin/day, 200 μg hIGF-I/day, or 20 μg insulin/day plus 200 μg hIGF-I/day, for 10 days with the animals being killed 2–3 h after the final injection. Hypoglycaemia was not observed in any of the treatment groups. hIGF-I treatment increased longitudinal growth and weight gain (P<0·05), while insulin treatment had no effect. Plasma IGF-I levels were increased in groups treated with hIGF-I (P<0·05), while insulin treatment resulted in a reduction (P<0-05): saline=267·1 ± 15·6 (ng/ml ± s.e.m.), insulin=219·3 ± 17·5, hIGF-I=391·7 ± 17·6, insulin plus hIGF-I=357·5 ± 31·8. Hepatic IGF-I mRNA expression was increased in insulin-treated dw/dw rats in comparison with hIGF-I-treated animals (P<0·05) but not in comparison with saline control or the combined treatment groups. Plasma levels of intact IGFBP-3, measured by ligand blot analysis, were increased in all treatment groups compared with saline (P<0·05): saline=100·0 ± 9·4% (% of saline ± s.e.m.), insulin=149·9 ± 17·5%, hIGF-I= 191·4 ± 17·3%, insulin plus hIGF-I=205·4 ± 15·3%. The levels of the 28/32 kDa IGFBPs and IGFBP-4 in plasma were increased by hIGF-I treatment (P<0·05) but not by insulin treatment. Hepatic specific 125I-bovine GH binding was not significantly different in any of the treatment groups. This study provides the first evidence in non-diabetic animals that insulin regulates hepatic IGF-I mRNA expression, plasma IGF-I and plasma IGFBP-3 levels in the GH-deficient state without changes in hepatic GH receptors. The divergent response of plasma IGF-I and IGFBP-3 levels to insulin treatment in the present study may indicate an effect of insulin on the clearance of IGF-I from the circulation. Journal of Endocrinology (1996) 150, 67–76

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Comparative study of insulin-like growth factor-I (IGF-I) and IGF-binding protein-3 (IGFBP-3) level and ratio measurements and their relationship with an index of clinical activity in the management of patients with acromegaly

Metabolism ◽

10.1016/s0026-0495(97)90183-9 ◽

1997 ◽

Vol 46 (5) ◽

pp. 494-498 ◽

Cited By ~ 16

Author(s):

Concepción Páramo ◽

M.Amalia Andrade O ◽

Enrique Fluiters ◽

Reyes Luna ◽

Javier de la Fuente ◽

...

Keyword(s):

Growth Factor ◽

Comparative Study ◽

Binding Protein ◽

Clinical Activity ◽

Insulin Like Growth Factor ◽

Factor I ◽

Igf I ◽

Igf Binding ◽

Igf Binding Protein ◽

Igfbp 3

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Specimen processing time and measurement of total insulin-like growth factor-I (IGF-I), free IGF-I, and IGF binding protein-3 (IGFBP-3)

Growth Hormone & IGF Research ◽

10.1016/j.ghir.2006.01.002 ◽

2006 ◽

Vol 16 (2) ◽

pp. 86-92 ◽

Cited By ~ 15

Author(s):

Tiffany G. Harris ◽

Howard D. Strickler ◽

Herbert Yu ◽

Michael N. Pollak ◽

E. Scott Monrad ◽

...

Keyword(s):

Growth Factor ◽

Processing Time ◽

Binding Protein ◽

Insulin Like Growth Factor ◽

Factor I ◽

Igf I ◽

Specimen Processing ◽

Igf Binding ◽

Igf Binding Protein ◽

Igfbp 3

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Dexamethasone administration attenuates the inhibitory effect of lipopolysaccharide on IGF-I and IGF-binding protein-3 in adult rats

Journal of Endocrinology ◽

10.1677/joe.1.06109 ◽

2005 ◽

Vol 185 (3) ◽

pp. 467-476 ◽

Cited By ~ 2

Author(s):

Teresa Priego ◽

Miriam Granado ◽

Ana Isabel Martín ◽

Asunción López-Calderón ◽

María Angeles Villanúa

Keyword(s):

Gene Expression ◽

Inhibitory Effect ◽

Mrna Levels ◽

Serum Concentrations ◽

Gh Receptor ◽

Its Gene ◽

Igf I ◽

Igf Binding ◽

Igf Binding Protein ◽

Igfbp 3

The aim of this study was to investigate whether glucocorticoid administration had a beneficial effect on serum concentrations of insulin-like growth factor I (IGF-I) and on IGF-binding protein 3 (IGFBP-3) in rats injected with lipopolysaccharide (LPS). Adult male rats were injected with LPS or saline and pretreated with dexamethasone or saline. Dexamethasone administration decreased growth hormone (GH) receptor and IGF-I mRNA levels in the liver of control rats. LPS decreased GH receptor and IGF-I gene expression in the liver of saline-treated rats but not in the liver of dexamethasone-pretreated rats. In the kidney, GH receptor mRNA levels were not modified by dexamethasone or LPS treatment. However, LPS decreased renal IGF-I gene expression and dexamethasone pretreatment prevented this decrease. Serum concentrations of IGF-I were decreased by LPS, and dexamethasone pretreatment attenuated this effect. The gene expression of IGFBP-3 in the liver and kidney and its circulating levels were decreased by LPS. In control rats dexamethasone increased circulating IGFBP-3 and its gene expression in the liver, and decreased the proteolysis of this protein. Dexamethasone pretreatment attenuated the LPS-induced decrease in IGFBP-3 gene expression in the liver and prevented the LPS-induced decrease in IGFBP-3 gene expression in the kidney. Moreover, dexamethasone pretreatment attenuated the LPS-induced decrease in serum concentrations of IGFBP-3 and decreased the LPS-induced IGFBP-3 proteolysis in serum. In conclusion, dexamethasone pretreatment partially attenuates the inhibitory effect of LPS on serum IGF-I by blocking the decrease of its gene expression in the kidney as well as by attenuating the decrease in serum concentrations of IGFBP-3.

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