The stimulatory effect of growth hormone, prolactin, and placental lactogen on beta-cell proliferation is not mediated by insulin-like growth factor-I

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Standard

The stimulatory effect of growth hormone, prolactin, and placental lactogen on beta-cell proliferation is not mediated by insulin-like growth factor-I. / Billestrup, N; Nielsen, Jens Høiriis.

I: Endocrinology, Bind 129, Nr. 2, 08.1991, s. 883-8.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Billestrup, N & Nielsen, JH 1991, 'The stimulatory effect of growth hormone, prolactin, and placental lactogen on beta-cell proliferation is not mediated by insulin-like growth factor-I', Endocrinology, bind 129, nr. 2, s. 883-8.

APA

Billestrup, N., & Nielsen, J. H. (1991). The stimulatory effect of growth hormone, prolactin, and placental lactogen on beta-cell proliferation is not mediated by insulin-like growth factor-I. Endocrinology, 129(2), 883-8.

Vancouver

Billestrup N, Nielsen JH. The stimulatory effect of growth hormone, prolactin, and placental lactogen on beta-cell proliferation is not mediated by insulin-like growth factor-I. Endocrinology. 1991 aug;129(2):883-8.

Author

Billestrup, N ; Nielsen, Jens Høiriis. / The stimulatory effect of growth hormone, prolactin, and placental lactogen on beta-cell proliferation is not mediated by insulin-like growth factor-I. I: Endocrinology. 1991 ; Bind 129, Nr. 2. s. 883-8.

Bibtex

@article{ae6c4c5b2b1e432f9ab3c36fbf1e0371,
title = "The stimulatory effect of growth hormone, prolactin, and placental lactogen on beta-cell proliferation is not mediated by insulin-like growth factor-I",
abstract = "The effects of GH, PRL, and placental lactogen (PL) on the proliferation of pancreatic beta-cells in vitro were studied as well as the possible effect of insulin-like growth factor-I (IGF-I) in mediating this effect. Proliferating beta-cells were identified by staining with a monoclonal antibody to bromodeoxyuridine (BrdU) after cells were incubated for 1 h in the presence of 10 microM BrdU. By double staining with insulin antibodies it was found that 6.3{\%} of the beta-cells had incorporated BrdU when cultured for 7 days in the presence of 1 microgram/ml human GH (hGH) compared to 0.6{\%} when cultured in the absence of hGH. Similar results were obtained using rat GH. The half-maximal effect of hGH on beta-cell proliferation was observed at 10 ng/ml, and the maximal effect at 100 ng/ml. Islet cells cultured in the presence of PRL or PL caused a dose-dependent increase in beta-cell proliferation similar to that caused by hGH. GH, PRL, and PL had no effect on the proliferation of glucagon- or somatostatin-producing cells. The addition of 100 ng/ml IGF-I to either control or GH-stimulated islet cells did not affect the labeling index. When GH-stimulated proliferation of beta-cells was measured in the presence of neutralizing concentrations of a rabbit IGF-I antiserum, the percentage of beta-cells incorporating BrdU was unaffected. Using Northern blot analysis, no IGF-I transcripts could be detected in RNA from GH-stimulated islets, whereas IGF-I transcripts were readily detected in RNA isolated from rat liver tissue. These data suggest that the stimulatory effect of GH, PRL, and PL on beta-cell proliferation is not mediated by IGF-I, but, rather, is a direct mitogenic effect on the beta-cell.",
keywords = "Animals, Bromodeoxyuridine, Cell Division, Gene Expression, Glucagon, Growth Hormone, Immune Sera, Insulin-Like Growth Factor I, Islets of Langerhans, Placental Lactogen, Prolactin, Rats, Rats, Inbred Strains, Recombinant Proteins, Somatostatin",
author = "N Billestrup and Nielsen, {Jens H{\o}iriis}",
year = "1991",
month = "8",
language = "English",
volume = "129",
pages = "883--8",
journal = "Endocrinology",
issn = "0013-7227",
publisher = "Oxford University Press",
number = "2",

}

RIS

TY - JOUR

T1 - The stimulatory effect of growth hormone, prolactin, and placental lactogen on beta-cell proliferation is not mediated by insulin-like growth factor-I

AU - Billestrup, N

AU - Nielsen, Jens Høiriis

PY - 1991/8

Y1 - 1991/8

N2 - The effects of GH, PRL, and placental lactogen (PL) on the proliferation of pancreatic beta-cells in vitro were studied as well as the possible effect of insulin-like growth factor-I (IGF-I) in mediating this effect. Proliferating beta-cells were identified by staining with a monoclonal antibody to bromodeoxyuridine (BrdU) after cells were incubated for 1 h in the presence of 10 microM BrdU. By double staining with insulin antibodies it was found that 6.3% of the beta-cells had incorporated BrdU when cultured for 7 days in the presence of 1 microgram/ml human GH (hGH) compared to 0.6% when cultured in the absence of hGH. Similar results were obtained using rat GH. The half-maximal effect of hGH on beta-cell proliferation was observed at 10 ng/ml, and the maximal effect at 100 ng/ml. Islet cells cultured in the presence of PRL or PL caused a dose-dependent increase in beta-cell proliferation similar to that caused by hGH. GH, PRL, and PL had no effect on the proliferation of glucagon- or somatostatin-producing cells. The addition of 100 ng/ml IGF-I to either control or GH-stimulated islet cells did not affect the labeling index. When GH-stimulated proliferation of beta-cells was measured in the presence of neutralizing concentrations of a rabbit IGF-I antiserum, the percentage of beta-cells incorporating BrdU was unaffected. Using Northern blot analysis, no IGF-I transcripts could be detected in RNA from GH-stimulated islets, whereas IGF-I transcripts were readily detected in RNA isolated from rat liver tissue. These data suggest that the stimulatory effect of GH, PRL, and PL on beta-cell proliferation is not mediated by IGF-I, but, rather, is a direct mitogenic effect on the beta-cell.

AB - The effects of GH, PRL, and placental lactogen (PL) on the proliferation of pancreatic beta-cells in vitro were studied as well as the possible effect of insulin-like growth factor-I (IGF-I) in mediating this effect. Proliferating beta-cells were identified by staining with a monoclonal antibody to bromodeoxyuridine (BrdU) after cells were incubated for 1 h in the presence of 10 microM BrdU. By double staining with insulin antibodies it was found that 6.3% of the beta-cells had incorporated BrdU when cultured for 7 days in the presence of 1 microgram/ml human GH (hGH) compared to 0.6% when cultured in the absence of hGH. Similar results were obtained using rat GH. The half-maximal effect of hGH on beta-cell proliferation was observed at 10 ng/ml, and the maximal effect at 100 ng/ml. Islet cells cultured in the presence of PRL or PL caused a dose-dependent increase in beta-cell proliferation similar to that caused by hGH. GH, PRL, and PL had no effect on the proliferation of glucagon- or somatostatin-producing cells. The addition of 100 ng/ml IGF-I to either control or GH-stimulated islet cells did not affect the labeling index. When GH-stimulated proliferation of beta-cells was measured in the presence of neutralizing concentrations of a rabbit IGF-I antiserum, the percentage of beta-cells incorporating BrdU was unaffected. Using Northern blot analysis, no IGF-I transcripts could be detected in RNA from GH-stimulated islets, whereas IGF-I transcripts were readily detected in RNA isolated from rat liver tissue. These data suggest that the stimulatory effect of GH, PRL, and PL on beta-cell proliferation is not mediated by IGF-I, but, rather, is a direct mitogenic effect on the beta-cell.

KW - Animals

KW - Bromodeoxyuridine

KW - Cell Division

KW - Gene Expression

KW - Glucagon

KW - Growth Hormone

KW - Immune Sera

KW - Insulin-Like Growth Factor I

KW - Islets of Langerhans

KW - Placental Lactogen

KW - Prolactin

KW - Rats

KW - Rats, Inbred Strains

KW - Recombinant Proteins

KW - Somatostatin

M3 - Journal article

C2 - 1677331

VL - 129

SP - 883

EP - 888

JO - Endocrinology

JF - Endocrinology

SN - 0013-7227

IS - 2

ER -

ID: 47973788