Inhibition of Access of Bound Somatomedin to Membrane Receptor and Immunobinding Sites: A Comparison of Radioreceptor and Radioimmunoassay of Somatomedin in Native and Acid-Ethanol-Extracted Serum*

Daughaday, William H.; Mariz, Ida K.; Blethen, Sandra L.

doi:10.1210/jcem-51-4-781

Cited by 784 publications

(352 citation statements)

References 18 publications

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“…A significant fall in GH levels, induced by the GH-RH antagonists, could, through mechanisms involving suppression of IGFs, be of major importance for the inhibition of tumour growth. Measurements of serum IGF levels can be affected by the presence of IGF-binding proteins, but our assays were performed after acid-ethanol cryoprecipitation extraction (Breier et al, 1991;Daughaday et al, 1980). Recently, Lee et al (1996) examined acid-ethanol extraction and acid-chromatography procedure for IGF and reported that the results were nearly identical.…”

Section: Discussionmentioning

confidence: 99%

“…Their results show that IGF-I levels found after acid-ethanol extraction are similar to those obtained by HPLC. Crawford et al (1992) also indicated that the acid-ethanol extraction method of Daughaday et al (1980), originally validated for human serum, is also satisfactory for use with rat serum. Our work shows that, in nude mice treated with the GH-RH antagonist MZ-4-71, serum IGF-I levels were significantly lower compared with control animals.…”

Section: Discussionmentioning

confidence: 99%

“…All serum and reconstituted tissue samples for IGF-I and IGF-II determination were extracted by a modified acid-ethanol cryoprecipitation method described previously (Daughaday et al, 1980;Breier et al, 1991). This method eliminates most of the IGF binding proteins, which can interfere in the radioimmunoassay (RIA).…”

Section: Radioimmunoassays Of Gh Igf-i and Igf-iimentioning

confidence: 99%

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Inhibition of in vivo proliferation of androgen-independent prostate cancers by an antagonist of growth hormone-releasing hormone

Jungwirth

Schally²,

Pinski³

et al. 1997

Br J Cancer

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Summary Tumour-inhibitory effects of a new antagonist of growth hormone-releasing hormone (GH-RH), MZ-4-71, were evaluated in nude mice bearing androgen-independent human prostate cancer cell lines DU-145 and PC-3 and in Copenhagen rats implanted with Dunning R-3327 AT-1 prostatic adenocarcinoma. After 6 weeks of therapy, the tumour volume in nude mice with DU-1 45 prostate cancers treated with 40 ,ug day-' MZ-4-71 was significantly decreased to 37 ± 13 mm3 (P < 0.01) compared with controls that measured 194 ± 35 mm3. A similar inhibition of tumour growth was obtained in nude mice bearing PC-3 cancers, in which the treatment with MZ-4-71 for 4 weeks diminished the tumour volume to 1 19 ± 35 mm3 compared with 397 ± 115 mm3 for control animals. Therapy with MZ-4-71 also significantly decreased weights of PC-3 and DU-145 tumours and increased tumour doubling time. Serum levels of GH and IGF-I were significantly decreased in animals treated with GH-RH antagonist. In PC-3 tumour tissue, the levels of IGF-I and IGF-II were reduced to non-detectable values after therapy with MZ-4-71. The growth of Dunning R-3327 AT-1 tumours in rats was also significantly inhibited after 3 weeks of treatment with 100 gg of MZ-4-71 day-' i.p. as shown by a reduction in tumour volume and weight (both P-values < 0.05). Specific high-affinity binding sites for IGF-I were found on the membranes of DU-145, PC-3 and Dunning R-3327 AT-1 tumours. Our results indicate that GH-RH antagonist MZ-4-71 suppresses growth of PC-3, DU-145 and Dunning AT-I androgen-independent prostate cancers, through diminution of GH release and the resulting decrease in the secretion of hepatic IGF-I, or through mechanisms involving a lowering of tumour IGF-I levels and possibly an inhibition of tumour IGF-I and IGF-Il production. GH-RH antagonists could be considered for further development for the therapy of prostate cancer, especially after the relapse.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Radioimmunoassays Of Gh Igf-i and Igf-iimentioning

confidence: 99%

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Inhibition of in vivo proliferation of androgen-independent prostate cancers by an antagonist of growth hormone-releasing hormone

Jungwirth

Schally²,

Pinski³

et al. 1997

Br J Cancer

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“…Total IGF-I levels were determined in the samples by RIA after serum extraction by the acid-ethanol method [20]. For assay purposes, hrIGF-I (Bachem Inc., Torrance, Calif., USA) was used as standard and tracer.…”

Section: Igf-i Assaymentioning

confidence: 99%

Relationship between non-enzymatic glycosylation and changes in serum insulin-like growth factor-1 (IGF-1) and IGF-binding protein-3 levels in patients with type 2 diabetes mellitus

et al. 1998

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The possible occurrence of increased non-enzymatic glycosylation of serum insulin-like growth factor binding protein-3 (IGFBP-3) in vivo and the changes that would simultaneously occur in serum levels of IGFBP-3 and insulin-like growth factor-1 (IGF-I) were investigated. We measured levels of IGF-I and IGFBP-3 and the degree of glycation of total serum protein and IGFBP-3, in serum samples obtained from patients with poorly controlled noninsulin-dependent diabetes (type 2) and from age-matched non-diabetic controls. Type 2 diabetic patients had significantly higher glycated serum protein (GlyP) levels. GlyP significantly correlated with age in the control (r = 0.315, P < 0.05) but not in the type 2 diabetes group. Control and diabetic subjects had comparable serum IGF-I levels and in both groups IGF-I levels tended to decrease with age (r = -0.567, P < 0.001 and r = -0.465, P < 0.05 for control and type 2 diabetic subjects, respectively). In the type 2 diabetes group, IGF-I levels showed a negative correlation with serum GlyP values (r = -0.476, P < 0.05). Type 2 diabetic and control patients had comparable serum IGFBP-3 levels, which were significantly higher in diabetic patients in the older age subgroups. A negative correlation was found between IGFBP-3 levels and age in the control (r = -0.705, P < 0.001) and in the type 2 diabetes groups (r = -0.463, P < 0.05). A significant negative correlation was found between IGFBP-3 levels and GlyP in control (r = -0.449, P < 0.002) but not in type 2 diabetic subjects. The mean glycated IGFBP-3 (GlyIGFBP-3) levels were higher in the oldest type 2 diabetic patients. In these patients, GlyIGFBP-3 was negatively associated with IGF-I levels (r = -0.447, P < 0.05). The IGF-I/IGFBP-3 molar ratio was significantly reduced in the 46-60-year-old type 2 diabetic group, whereas the IGF-I/IGFBP-3 ratio was positively and significantly correlated with GlyP levels only in the control group (r = 0.489, P < 0.01). Our results show that: a) increased non-enzymatic glycosylation of IGFBP-3 occurs in vivo; and b) this effect is accompanied by an increase in IGFBP-3 levels. These results suggest that the IGF-I/IGFBP-3 system is another target for the metabolic derangements of type 2 diabetes. Its alterations might play a role in diabetic complications.

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“…Insulin was measured using the Insulin Radioimmunoassay kit from Bio-RIA. Somatomedin-C levels were determined on acid-ethanol extracted serum samples [16] by specific radioimmunoassay using antiserum Tr4 as described previously [17]. Glucose was measured using glucose oxidase and peroxidase.…”

Section: Hormone Assaysmentioning

confidence: 99%

Adrenal involvement in the diabetes-induced loss of growth hormone and prolactin receptors in the livers of female rats

Bryson

Baxter

1986

Diabetologia

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Summary. Streptozotocin-induced diabetes causes a decrease in growth hormone and prolactin receptors in the livers of female rats, and in the serum concentration of somatomedin-C/ insulin-like growth factor-I, concomitantly with an increase in the serum testosterone levels. In this study, a possible role for adrenal androgens in the loss of receptors was examined. Rats were adrenalectomised bilaterally 3 days after the induction of diabetes with streptozotocin (100mg/kg intravenously), and livers were removed 3 days later. Adrenalectomy had no effect on binding of ovine prolactin or bovine growth hormone to liver microsomal membranes from non-diabetic rats, but in diabetic rats it entirely abolished the 56% decrease in prolactin binding and significantly reversed the 66% decrease in growth hormone binding and the parallel fall in serum levels of somatomedin-C/insulin-like growth factor-I (p<0.05). Adrenalectomy also prevented the diabetes-induced rise in serum testosterone. Daily injection of testosterone to normal and diabetic rats for 12 days significantly reduced both prolactin and growth hormone binding (p< 0.001), with the effect of diabetes being additive upon the testosterone effect. Implantation of testosterone-filled silastic capsules at the time of adrenalectomy (i. e. for 3 days) did not prevent the adrenalectomy-induced restoration of both growth hormone and prolactin receptors. The resulting high serum testosterone level did not reduce binding to growth hormone receptors in control rats over the 3 day period, and caused no further decrease in diabetic rats. However, binding to prolactin receptors was reduced by 47% in control animals with no further loss in diabetic animals (p < 0.001). Adrenalectomy prevented the loss of prolactin receptors in both testosterone-treated and diabetic rats. These results indicate that, whether or not the rise in testosterone of adrenal origin contributes to the receptor loss in diabetes, the effect also depends on another factor of adrenal origin.

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Inhibition of Access of Bound Somatomedin to Membrane Receptor and Immunobinding Sites: A Comparison of Radioreceptor and Radioimmunoassay of Somatomedin in Native and Acid-Ethanol-Extracted Serum*

Cited by 784 publications

References 18 publications

Inhibition of in vivo proliferation of androgen-independent prostate cancers by an antagonist of growth hormone-releasing hormone

Inhibition of in vivo proliferation of androgen-independent prostate cancers by an antagonist of growth hormone-releasing hormone

Relationship between non-enzymatic glycosylation and changes in serum insulin-like growth factor-1 (IGF-1) and IGF-binding protein-3 levels in patients with type 2 diabetes mellitus

Adrenal involvement in the diabetes-induced loss of growth hormone and prolactin receptors in the livers of female rats

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