The Measurement of Insulin-Like Growth Factor I: Clinical Applications and Significance

Teale, J D

doi:10.1177/000456328602300406

Cited by 65 publications

(26 citation statements)

References 61 publications

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“…Thereafter, plasma IGF-I declines steadily until normal adult values are reached (12,25). After 40 y of age, IGF-I declines again to levels lower than in early adulthood (26).…”

Section: Discussion Table 4 Correlation Of Individual Concentrationsmentioning

confidence: 97%

“…The pattern of IGF-I development from childhood to adult life has been more consistently established (8,12,26). Although the methodologies are still evolving, the plasma IGF-I concentration typically increases with age in young children (>10.3 nM or 80 /Lg/L) with a prominent surge (>51 nM or 400 /LgIL) at puberty (20,27).…”

Section: Discussion Table 4 Correlation Of Individual Concentrationsmentioning

confidence: 99%

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Insulin-Like Growth Factor (IGF)-I and IGF-Binding Protein 3 during the First Year in Term and Preterm Infants

et al. 1995

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Plasma IGF-I and IGF-binding protein 3 (IGFBP-3) were determined by radioimmunoassay in term infants (n = 51) at 0, 2,4, 6, and 12 mo and preterm infants (n = 51) at -3 (28.4 wk postconceptional age), -2, -1.5, -1,0,2,4,6,9, and 12 rna from expected term. The effects of gestational age at birth (term or preterm) and study age were determined by repeated measures analysis of variance and Fisher's least squares difference. In preterm infants, IGF-I increased between -3 and 2 mo from 0.75 to 10.4 nM, decreased between 2 and 9 mo to 7.3 nM, and increased again between 9 and 12 mo to 10.1 nM (p < 0.0001), whereas IGFBP-3 increased relatively little from -3 to 0 rna (14.2 to 30.2 nM, p < 0.05) and plateaued from 2 to 12 mo (49.8 to 62.3 nM). At 0 rna, IGF-I and IGFBP-3 were the same in term and preterm infants, but preterm infants had higher IGF-I from 2 IGF mediate the growth-promoting actions of growth hormone in regulating the proliferation and differentiation of different cell types (1). These polypeptides which are structurally homologous to insulin also exert insulin-like metabolic effects. Both these effects are mediated through target cell surface receptors (2). Most tissues in the body produce IGF, and they are present in serum mostly bound to specific high molecular weight binding proteins (3). Of the six IGFBP that have been identified so far, IGFBP-3 is the major form present in the serum (1, 2) and demonstrates a high affinity for both IGF-I and IGF-II. IGFBP-3 can exhibit either an inhibitory (4) or a potentiating (5) effect on IGF-I bioactivity in vitro, depending on its ability to alter the equilibrium between IGF-I and its receptor (5).

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“…Thereafter, plasma IGF-I declines steadily until normal adult values are reached (12,25). After 40 y of age, IGF-I declines again to levels lower than in early adulthood (26).…”

Section: Discussion Table 4 Correlation Of Individual Concentrationsmentioning

confidence: 97%

Section: Discussion Table 4 Correlation Of Individual Concentrationsmentioning

confidence: 99%

Insulin-Like Growth Factor (IGF)-I and IGF-Binding Protein 3 during the First Year in Term and Preterm Infants

et al. 1995

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“…We postulated that the discrepancies observed in the circulating levels of GH and IGF-I in the combination group can be explained by the fact that stimuli other than GH, such as prolactin (PRL), platelet-derived growth factor, or nutritional status, can also lead to an increase in IGF-I synthesis (30,31). Dardenne et al (32) reported that cells expressing GH receptor also express receptors for PRL.…”

Section: Discussionmentioning

confidence: 99%

Activation of growth hormone releasing hormone (GHRH) receptor stimulates cardiac reverse remodeling after myocardial infarction (MI)

Kanashiro‐Takeuchi

Takeuchi

Rick³

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

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Both cardiac myocytes and cardiac stem cells (CSCs) express the receptor of growth hormone releasing hormone (GHRH), activation of which improves injury responses after myocardial infarction (MI). Here we show that a GHRH-agonist (GHRH-A; JI-38) reverses ventricular remodeling and enhances functional recovery in the setting of chronic MI. This response is mediated entirely by activation of GHRH receptor (GHRHR), as demonstrated by the use of a highly selective GHRH antagonist (MIA-602). One month after MI, animals were randomly assigned to receive: placebo, GHRH-A (JI-38), rat recombinant GH, MIA-602, or a combination of GHRH-A and MIA-602, for a 4-wk period. We assessed cardiac performance and hemodynamics by using echocardiography and micromanometry derived pressure-volume loops. Morphometric measurements were carried out to determine MI size and capillary density, and the expression of GHRHR was assessed by immunofluorescence and quantitative RT-PCR. GHRH-A markedly improved cardiac function as shown by echocardiographic and hemodynamic parameters. MI size was substantially reduced, whereas myocyte and nonmyocyte mitosis was markedly increased by GHRH-A. These effects occurred without increases in circulating levels of growth hormone and insulin-like growth factor I and were, at least partially, nullified by GHRH antagonism, confirming a receptor-mediated mechanism. GHRH-A stimulated CSCs proliferation ex vivo, in a manner offset by MIA-602. Collectively, our findings reveal the importance of the GHRH signaling pathway within the heart. Therapy with GHRH-A although initiated 1 mo after MI substantially improved cardiac performance and reduced infarct size, suggesting a regenerative process. Therefore, activation of GHRHR provides a unique therapeutic approach to reverse remodeling after MI.heart failure | cardiac stem cells | cardiac regeneration

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“…Samples of medium and patients' serum underwent acid ethanol extraction with 2 N hydrochloric acid: absolute ethanol, 1:7 and were neutralised with Tris buffer. Duplicate aliquots were assayed using anti-IGF-I monoclonal antibody BPL-M23 as previously described (Teale & Marks, 1986;. Analysis of variance and Dunnett's test were used to assess the significance of differences in NSE and IGF-I levels before and during octreotide therapy.…”

Section: Growth Assaysmentioning

confidence: 99%

Experimental and clinical studies with somatostatin analogue octreotide in small cell lung cancer

Macaulay

Smith²,

Everard³

et al. 1991

Br J Cancer

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Summary We have detected somatostatin receptors (SSR) by autoradiography in 3/4 established small cell lung cancer (SCLC) cell lines but not in two non-SCLC cell lines. The growth of 1/3 SSR positive SCLC cell lines was significantly inhibited by the long-acting somatostatin analogue octreotide statin) 10-9M. We treated 20 SCLC patients with octreotide 250 gg three times daily for I week prechemotherapy (six patients) or at relapse after chemotherapy (14). Octreotide was well tolerated, and serum insulin-like growth factor-I levels were suppressed to 62±7% of pre-treatment levels. However there was no evidence of anti-tumour activity measured by tumour bulk or serum levels of neuron-specific enolase. In one patient metastatic skin nodules were shown to be SSR positive before and at the end of 2 weeks octreotide. Despite this the patient had progressive disease, and tumour cells obtained by fine needle aspirate before and after treatment showed no growth inhibition when cultured with octreotide immediately or following establishment as a cell line. In summary we saw little correlation between SSR expression and growth inhibition by octreotide, either in vitro or clinically.Somatostatins are a family of 14-and 28-residue neuropeptides which regulate peptide secretion from the pituitary, gut and pancreas (Bloom & Polak, 1987;Frohman & Krieger, 1987). Somatostatin receptors (SSR) are expressed by these so-called 'SS target tissues', and by tumours arising from them including pituitary adenomas and pancreatic insulinomas (Reubi et al., 1982;1984). Natural SS-14 is of limited therapeutic use here because of its short plasma half-life (3 min) and diverse action (Moreau & DeFeudis, 1987;Schally, 1988). Systematic structure/activity studies have led to the development of potent octapeptide SS analogues with prolonged and selective activity. One of these, octreotide (SMS 201-995, Sandostatin) has pharmacological effects in vivo for up to 9 h and is 45-70 times more potent than SS-14 at inhibiting growth hormone release (Plewe et al., 1987;Schally, 1988). In patients with acromegaly, carcinoid syndrome, insulinomas and other gastroenteropancreatic tumours, octreotide produces clinical improvement in parallel with suppression of inappropriate peptide secretion, and in some cases reduction in tumour bulk Wood et al., 1985;Kvols et al., 1986;Lamberts et al., 1987;Comi, 1989;Maton, 1989). Octreotide and other octapeptide SS analogues have also shown experimental evidence of antiproliferative activity in some common solid tumours, including cancers of the breast, exocrine pancreas, colon and prostate (Setyono-Han et al., 1987;Schally, 1988;Parmar et al., 1989;Weber et al., 1989). Growth inhibition here could be mediated directly, via SSR which have been detected on breast, pancreas and prostate cancers (Reubi et al., 1987;Setyono-Han et al., 1987;Srkalovic et al., 1990), or indirectly via suppression of local or circulating levels of growth factors (Schally, 1988).There is some evidence that SS may play a role in growth regulat...

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The Measurement of Insulin-Like Growth Factor I: Clinical Applications and Significance

Cited by 65 publications

References 61 publications

Insulin-Like Growth Factor (IGF)-I and IGF-Binding Protein 3 during the First Year in Term and Preterm Infants

Insulin-Like Growth Factor (IGF)-I and IGF-Binding Protein 3 during the First Year in Term and Preterm Infants

Activation of growth hormone releasing hormone (GHRH) receptor stimulates cardiac reverse remodeling after myocardial infarction (MI)

Experimental and clinical studies with somatostatin analogue octreotide in small cell lung cancer

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