Effects of sex and pregnancy hormones on growth hormone and prolactin receptor gene expression in insulin-producing cells

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Standard

Effects of sex and pregnancy hormones on growth hormone and prolactin receptor gene expression in insulin-producing cells. / Møldrup, Annette; Petersen, Elisabeth D.; Nielsen, Jens Høiriis.

I: Endocrinology, Bind 133, Nr. 3, 09.1993, s. 1165-72.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Møldrup, A, Petersen, ED & Nielsen, JH 1993, 'Effects of sex and pregnancy hormones on growth hormone and prolactin receptor gene expression in insulin-producing cells', Endocrinology, bind 133, nr. 3, s. 1165-72.

APA

Møldrup, A., Petersen, E. D., & Nielsen, J. H. (1993). Effects of sex and pregnancy hormones on growth hormone and prolactin receptor gene expression in insulin-producing cells. Endocrinology, 133(3), 1165-72.

Vancouver

Møldrup A, Petersen ED, Nielsen JH. Effects of sex and pregnancy hormones on growth hormone and prolactin receptor gene expression in insulin-producing cells. Endocrinology. 1993 sep;133(3):1165-72.

Author

Møldrup, Annette ; Petersen, Elisabeth D. ; Nielsen, Jens Høiriis. / Effects of sex and pregnancy hormones on growth hormone and prolactin receptor gene expression in insulin-producing cells. I: Endocrinology. 1993 ; Bind 133, Nr. 3. s. 1165-72.

Bibtex

@article{0ef1208fa65c476daed01407613501c0,
title = "Effects of sex and pregnancy hormones on growth hormone and prolactin receptor gene expression in insulin-producing cells",
abstract = "During pregnancy, marked hyperplasia of the pancreatic islet cells has been observed. This effect may be mediated by the pregnancy-associated peptide hormones, placental lactogen, PRL, and GH, which were previously shown to be mitogenic to beta-cells in vitro. To study whether the responsiveness of islet cells to these hormones is regulated on the receptor level, GH and PRL receptor gene expression was studied in pancreata from male rats and virgin, pregnant, and lactating female rats and in cultured islets and insulinoma cells (RIN-5AH) in response to various hormones. The mRNA levels were quantitated by ribonuclease protection assay, using probes specific for mRNA encoding, extracellular and intracellular domains of the GH receptor, and short and long forms of the PRL receptor, respectively. Specific transcripts for the GH receptor were present in pancreas, islets, and RIN-5AH cells. Furthermore, as previously observed in RIN-5AH cells, a predominant expression of the long form of PRL receptor vs. the short form was also found in pancreas and islet cells. Male and nonpregnant female pancreas did not differ significantly in their levels of GH and PRL receptor mRNAs. On day 14 of pregnancy, increases in both GH and PRL receptor mRNA levels were observed (1.7- and 2.4-fold, respectively), and a further increase occurred in late pregnancy (day 19), when GH and PRL receptor mRNA levels were 2.7- and 3.9-fold higher than those in the nonpregnant state. mRNA levels returned toward the basal level during lactation. In the cultured islets, PRL receptor mRNA levels were markedly increased by GH and PRL (3.5- and 6.5-fold, respectively) after exposure for 24 h, whereas estradiol and testosterone had modest stimulating effects (1.8- and 1.5-fold increases, respectively). Dexamethasone induced a 2.5-fold increase in GH receptor mRNA levels, and a weak stimulatory effect was also observed for progesterone. In RIN-5AH cells, the effect of dexamethasone on GH receptor mRNA was detectable after 2 h and maximal after 16 h. In contrast, the effects of GH and PRL on PRL receptor mRNA required 24-48 h of exposure. The effective doses were within the physiological ranges. In conclusion, these results show a differential hormonal regulation of GH and PRL receptor gene expression in the pancreatic islets, which may play a role in the adaptive beta-cell growth during pregnancy.",
keywords = "Animals, Animals, Newborn, Female, Gene Expression, Gonadal Steroid Hormones, Growth Hormone, Insulinoma, Islets of Langerhans, Kinetics, Lactation, Male, Pancreatic Neoplasms, Placental Lactogen, Pregnancy, Pregnancy Proteins, Prolactin, RNA, Messenger, Rats, Rats, Wistar, Receptors, Prolactin, Receptors, Somatotropin, Tumor Cells, Cultured",
author = "Annette M{\o}ldrup and Petersen, {Elisabeth D.} and Nielsen, {Jens H{\o}iriis}",
year = "1993",
month = sep,
language = "English",
volume = "133",
pages = "1165--72",
journal = "Endocrinology",
issn = "0013-7227",
publisher = "Oxford University Press",
number = "3",

}

RIS

TY - JOUR

T1 - Effects of sex and pregnancy hormones on growth hormone and prolactin receptor gene expression in insulin-producing cells

AU - Møldrup, Annette

AU - Petersen, Elisabeth D.

AU - Nielsen, Jens Høiriis

PY - 1993/9

Y1 - 1993/9

N2 - During pregnancy, marked hyperplasia of the pancreatic islet cells has been observed. This effect may be mediated by the pregnancy-associated peptide hormones, placental lactogen, PRL, and GH, which were previously shown to be mitogenic to beta-cells in vitro. To study whether the responsiveness of islet cells to these hormones is regulated on the receptor level, GH and PRL receptor gene expression was studied in pancreata from male rats and virgin, pregnant, and lactating female rats and in cultured islets and insulinoma cells (RIN-5AH) in response to various hormones. The mRNA levels were quantitated by ribonuclease protection assay, using probes specific for mRNA encoding, extracellular and intracellular domains of the GH receptor, and short and long forms of the PRL receptor, respectively. Specific transcripts for the GH receptor were present in pancreas, islets, and RIN-5AH cells. Furthermore, as previously observed in RIN-5AH cells, a predominant expression of the long form of PRL receptor vs. the short form was also found in pancreas and islet cells. Male and nonpregnant female pancreas did not differ significantly in their levels of GH and PRL receptor mRNAs. On day 14 of pregnancy, increases in both GH and PRL receptor mRNA levels were observed (1.7- and 2.4-fold, respectively), and a further increase occurred in late pregnancy (day 19), when GH and PRL receptor mRNA levels were 2.7- and 3.9-fold higher than those in the nonpregnant state. mRNA levels returned toward the basal level during lactation. In the cultured islets, PRL receptor mRNA levels were markedly increased by GH and PRL (3.5- and 6.5-fold, respectively) after exposure for 24 h, whereas estradiol and testosterone had modest stimulating effects (1.8- and 1.5-fold increases, respectively). Dexamethasone induced a 2.5-fold increase in GH receptor mRNA levels, and a weak stimulatory effect was also observed for progesterone. In RIN-5AH cells, the effect of dexamethasone on GH receptor mRNA was detectable after 2 h and maximal after 16 h. In contrast, the effects of GH and PRL on PRL receptor mRNA required 24-48 h of exposure. The effective doses were within the physiological ranges. In conclusion, these results show a differential hormonal regulation of GH and PRL receptor gene expression in the pancreatic islets, which may play a role in the adaptive beta-cell growth during pregnancy.

AB - During pregnancy, marked hyperplasia of the pancreatic islet cells has been observed. This effect may be mediated by the pregnancy-associated peptide hormones, placental lactogen, PRL, and GH, which were previously shown to be mitogenic to beta-cells in vitro. To study whether the responsiveness of islet cells to these hormones is regulated on the receptor level, GH and PRL receptor gene expression was studied in pancreata from male rats and virgin, pregnant, and lactating female rats and in cultured islets and insulinoma cells (RIN-5AH) in response to various hormones. The mRNA levels were quantitated by ribonuclease protection assay, using probes specific for mRNA encoding, extracellular and intracellular domains of the GH receptor, and short and long forms of the PRL receptor, respectively. Specific transcripts for the GH receptor were present in pancreas, islets, and RIN-5AH cells. Furthermore, as previously observed in RIN-5AH cells, a predominant expression of the long form of PRL receptor vs. the short form was also found in pancreas and islet cells. Male and nonpregnant female pancreas did not differ significantly in their levels of GH and PRL receptor mRNAs. On day 14 of pregnancy, increases in both GH and PRL receptor mRNA levels were observed (1.7- and 2.4-fold, respectively), and a further increase occurred in late pregnancy (day 19), when GH and PRL receptor mRNA levels were 2.7- and 3.9-fold higher than those in the nonpregnant state. mRNA levels returned toward the basal level during lactation. In the cultured islets, PRL receptor mRNA levels were markedly increased by GH and PRL (3.5- and 6.5-fold, respectively) after exposure for 24 h, whereas estradiol and testosterone had modest stimulating effects (1.8- and 1.5-fold increases, respectively). Dexamethasone induced a 2.5-fold increase in GH receptor mRNA levels, and a weak stimulatory effect was also observed for progesterone. In RIN-5AH cells, the effect of dexamethasone on GH receptor mRNA was detectable after 2 h and maximal after 16 h. In contrast, the effects of GH and PRL on PRL receptor mRNA required 24-48 h of exposure. The effective doses were within the physiological ranges. In conclusion, these results show a differential hormonal regulation of GH and PRL receptor gene expression in the pancreatic islets, which may play a role in the adaptive beta-cell growth during pregnancy.

KW - Animals

KW - Animals, Newborn

KW - Female

KW - Gene Expression

KW - Gonadal Steroid Hormones

KW - Growth Hormone

KW - Insulinoma

KW - Islets of Langerhans

KW - Kinetics

KW - Lactation

KW - Male

KW - Pancreatic Neoplasms

KW - Placental Lactogen

KW - Pregnancy

KW - Pregnancy Proteins

KW - Prolactin

KW - RNA, Messenger

KW - Rats

KW - Rats, Wistar

KW - Receptors, Prolactin

KW - Receptors, Somatotropin

KW - Tumor Cells, Cultured

M3 - Journal article

C2 - 8365359

VL - 133

SP - 1165

EP - 1172

JO - Endocrinology

JF - Endocrinology

SN - 0013-7227

IS - 3

ER -

ID: 47973322