The 25-KiloDalton Insulin-Like Growth Factor (IGF)-Binding Protein Inhibits both Basal and IGF-I-Mediated Growth of Chick Embryo Pelvic Cartilage<i>in Vitro</i>

Burch, Warner M.; Donate-Correa, Javier; Shively, John E.; Powell, David R.

doi:10.1210/jcem-70-1-173

Cited by 142 publications

(60 citation statements)

References 31 publications

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“…In the circulation of normal, non-pregnant individuals, IGFBP-1 is present as a highly phosphorylated form. Other studies have used either recombinant IGFBP-1 which is non-phosphorylated (Cox et al 1994, Lee et al 1996 or IGFBP-1 purified from amniotic fluid which is deficient in the highly phosphorylated form (Frauman et al 1989, Burch et al 1990, Angervo et al 1991, Liu et al 1991, Lewitt et al 1993. We therefore purified phosphorylated IGFBP-1 from HepG2-conditioned medium and found it was more potent than npIGFBP-1 since it completely reversed the effects of IGF-I at a 1:1 molar ratio, while at this molar ratio npIGFBP-1 did not significantly inhibit IGF mitogenic actions.…”

Section: Discussionmentioning

confidence: 99%

IGF-binding protein-1 inhibits IGF effects on adipocyte function: implications for insulin-like actions at the adipocyte

Siddals¹,

Westwood²,

Gibson³

et al. 2002

Journal of Endocrinology

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IGF action in vivo is acutely regulated by IGF-binding protein-1 (IGFBP-1) and its phosphorylation state is implicated in modulating these effects. Since IGFs have an important regulatory role in adipocyte function, we investigated the effects of phosphorylated IGFBP-1 (pIGFBP-1) and non-phosphorylated IGFBP-1 (npIGF BP-1) on 3T3-L1 preadipocyte proliferation and adipocyte metabolism.IGFs stimulated clonal expansion of 3T3-L1 cells (IGF-I more potently than IGF-II (EC 50 : 30 nM and 50 nM)). npIGFBP-1 inhibited IGF-I (50 nM) clonal expansion at a 5:1 molar ratio (P<0·01), whereas pIGFBP-1 (purified from HepG2 cell medium) abolished clonal expansion at a 1:1 molar ratio (P<0·005). In contrast, IGF-II-induced clonal expansion was inhibited 100% at a 1:1 molar ratio of npIGFBP-1.In mature adipocytes, IGF-I was equipotent with insulin in stimulating glucose uptake (EC 50 : 10 nM) and inhibiting isoproterenol-induced lipolysis (EC 50 : 15 nM). npIGFBP-1 completely reversed IGF-I effects at a 1:1 molar ratio (P<0·01).In summary, IGFs rather than insulin are potent regulators of clonal expansion in 3T3-L1 preadipocytes. Importantly, IGFs are equipotent with insulin in regulating adipocyte metabolism. IGFBP-1 inhibits IGF effects on preadipocyte proliferation and adipocyte metabolism, with pIGFBP-1 being more potent than npIGFBP-1 at inhibiting mitogenic actions. Since IGFBP-1 is acutely regulated by insulin, this could have important consequences in hyperinsulinaemic and insulin-resistant states.

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Section: Discussionmentioning

confidence: 99%

IGF-binding protein-1 inhibits IGF effects on adipocyte function: implications for insulin-like actions at the adipocyte

Siddals¹,

Westwood²,

Gibson³

et al. 2002

Journal of Endocrinology

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“…The synthesis and secretion of IGFBPs are thought to play important roles in the regulation of IGF hormonal action at the target cell level at a time when the extracellular concentration of IGF-I remains constant (33)(34)(35). Depending on the circumstances, IGFBPs can either inhibit (35) or stimulate (34) the action of IGF-I on mammalian cells, but their predominant Figure 7.…”

Section: Discussionmentioning

confidence: 99%

“…Depending on the circumstances, IGFBPs can either inhibit (35) or stimulate (34) the action of IGF-I on mammalian cells, but their predominant Figure 7. Effect of Ang II on the inhibitory effect of IGFBP-3 in hCG-induced PG production in perfused rabbit ovaries.…”

Section: Discussionmentioning

confidence: 99%

Interactions between insulin-like growth factor-I (IGF-I) and the renin-angiotensin system in follicular growth and ovulation.

Yoshimura¹,

Aoki²,

Sueoka³

et al. 1996

J. Clin. Invest.

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The interactions between insulin-like growth factor-I (IGF-I) and the renin-angiotensin system (RAS) in follicular growth and ovulation were studied with the use of an isolated perfused rabbit ovary preparation. Ovulation failed to occur in either control ovaries or the experimental ovaries perfused with IGF-I in a concentration of 1, 10, or 100 ng/ml in the absence of gonadotropin. Exposure to IGF-I stimulated the secretion rate of angiotensin II-like immunoreactivity (Ang II-IR) in perfused rabbit ovaries in a dose-dependent manner. The percent increase in follicle diameter in ovaries perfused with IGF-I for 12 h was significantly correlated with the secretion rate of Ang II-IR at 12 h after exposure to IGF-I. The addition of IGFBP-3 to the perfusate did not induce ovulation in the absence of gonadotropin, but exposure to IGFBP-3 inhibited hCG-induced ovulation in a dosedependent manner. In addition, IGFBP-3 significantly reduced the ovarian secretion rate of Ang II-IR and prostaglandins stimulated by hCG administration. Intrafollicular plasminogen activator (PA) activity significantly increased within 4 h after exposure to 100 ng/ml of IGF-I, compared with that in control ovaries perfused with medium alone. The concomitant addition of IGFBP-3 to the perfusate significantly reduced the IGF-I-stimulated PA activity in the preovulatory follicles at 4, 6, and 8 h after exposure to IGF-I. However, IGFBP-3 alone affected neither the ovarian secretion rate of Ang II-IR nor intrafollicular PA activity. Exposure to streptokinase, an exogenous PA, in vitro stimulated both follicular growth and the intrafollicular Ang II-IR content. In conclusion, IGF-I enhances both ovarian Ang II production and follicular development by stimulating intrafollicular PA activity. ( J. Clin. Invest. 1996. 98:308-316.)

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“…These relationships suggest that cortisol might influence fetal growth through modulation of fetal IGFBP-1 concentrations. It has been shown that plasma levels of IGFBP-1 correlate with IGF-inhibitory activity in diabetic serum (Taylor et al 1990) and IGFBP-1 inhibits the growth of chick embryo cartilage in vitro (Burch et al 1990). IGFBP-1 concentrations are also related to cortisol concentrations in newborns (Cianfarani et al 1998) and children (Martinelli et al 1999).…”

Section: Hormonesmentioning

confidence: 99%

The effect of a chronic maternal cortisol infusion on the late-gestation fetal sheep

Jensen¹,

Gallaher²,

Breier³

et al. 2002

Journal of Endocrinology

114

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Exposure of the fetus to excess maternal glucocorticoids has been postulated to alter fetal growth and development, and thus provide a possible mechanism for the link between impaired fetal growth and altered postnatal physiology. However, the effects of exposure to excess maternal glucocorticoids on fetal physiology and metabolism in utero have not been described. We therefore studied the effects of chronic maternal cortisol infusion on fetal growth, blood pressure, metabolism and endocrine status in chronically catheterised fetal sheep. We infused hydrocortisone (80 mg/day, n=6) or saline (n=8) for 10 days into the pregnant ewes beginning at 119 days of gestation. Maternal cortisol infusion reduced fetal growth rate by 30% (girth increment 2·9 0·3 vs 1·8 0·4 mm/ day, P=0·03). Maternal cortisol infusion increased fetal heart weight by 15% relative to body weight and increased ventricular wall thickness by 30% in the left and 50% in the right ventricle. The weight of the spleen was reduced by 30% and placental weight reduced by 25%. Fetal blood pressure increased by approximately 10 mmHg (20%) during maternal cortisol infusion.Maternal cortisol infusion did not alter amino-nitrogen concentrations. However, maternal lactate concentrations increased by 80% and fetal lactate concentrations increased by 74% with maternal cortisol infusion, and both maternal and fetal urea concentrations increased by 40%. Circulating maternal IGF-binding protein (IGFBP)-3 levels had increased by 20% by the end of the maternal cortisol infusion. Fetal IGF-I concentrations decreased during cortisol infusion and fetal IGFBP-1 concentrations were negatively correlated with fetal weight (r= 0·76, P=0·02).We conclude that even a modest elevation of maternal cortisol levels affects fetal growth, cardiovascular function, metabolism and endocrine status which may have longterm consequences.

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The 25-KiloDalton Insulin-Like Growth Factor (IGF)-Binding Protein Inhibits both Basal and IGF-I-Mediated Growth of Chick Embryo Pelvic Cartilagein Vitro

Cited by 142 publications

References 31 publications

IGF-binding protein-1 inhibits IGF effects on adipocyte function: implications for insulin-like actions at the adipocyte

IGF-binding protein-1 inhibits IGF effects on adipocyte function: implications for insulin-like actions at the adipocyte

Interactions between insulin-like growth factor-I (IGF-I) and the renin-angiotensin system in follicular growth and ovulation.

The effect of a chronic maternal cortisol infusion on the late-gestation fetal sheep

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