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Deletion of the G protein-coupled Receptor GPR30 Impairs Glucose Tolerance, Reduces Bone Growth, Increases Blood Pressure, and Eliminates Estradiol-stimulated Insulin Release in Female Mice.

Mårtensson, Ulrika LU ; Salehi, S Albert LU ; Windahl, Sara; Gomez, Maria LU ; Swärd, Karl LU ; Daszkiewicz-Nilsson, Joanna LU ; Wendt, Anna LU ; Andersson, Niklas; Hellstrand, Per LU and Grände, Per-Olof LU , et al. (2009) In Endocrinology 150(2). p.687-698
Abstract
In vitro studies suggest that the G protein-coupled receptor GPR30 is a functional estrogen receptor. However, the physiological role of GPR30 in vivo is unknown, and it remains to be determined if GPR30 is an estrogen receptor also in vivo. To this end, we studied the effects of disrupting the GPR30 gene in female and male mice. Female GPR30((-/-)) mice had hyperglycemia and impaired glucose tolerance, reduced body growth, increased blood pressure, and reduced serum insulin-like growth factor-I levels. The reduced growth correlated with a proportional decrease in skeletal development. The elevated blood pressure was associated with an increased vascular resistance manifested as an increased media:lumen ratio of the resistance arteries.... (More)
In vitro studies suggest that the G protein-coupled receptor GPR30 is a functional estrogen receptor. However, the physiological role of GPR30 in vivo is unknown, and it remains to be determined if GPR30 is an estrogen receptor also in vivo. To this end, we studied the effects of disrupting the GPR30 gene in female and male mice. Female GPR30((-/-)) mice had hyperglycemia and impaired glucose tolerance, reduced body growth, increased blood pressure, and reduced serum insulin-like growth factor-I levels. The reduced growth correlated with a proportional decrease in skeletal development. The elevated blood pressure was associated with an increased vascular resistance manifested as an increased media:lumen ratio of the resistance arteries. The hyperglycemia and impaired glucose tolerance in vivo were associated with decreased insulin expression and release in vivo and in vitro in isolated pancreatic islets. GPR30 is expressed in islets, and GPR30 deletion abolished estradiol-stimulated insulin release both in vivo in ovariectomized adult mice and in vitro in isolated islets. Our findings show that GPR30 is important for several metabolic functions in female mice including estradiol-stimulated insulin release. (Less)
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Contribution to journal
publication status
published
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Endocrinology
volume
150
issue
2
pages
687 - 698
publisher
Endocrine Society
external identifiers
  • wos:000262851200016
  • pmid:18845638
  • scopus:59649122739
ISSN
0013-7227
DOI
10.1210/en.2008-0623
language
English
LU publication?
yes
id
88635a63-05ce-43c5-ab63-0279f9a28757 (old id 1262362)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/18845638?dopt=Abstract
date added to LUP
2008-11-10 16:22:54
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2017-11-19 03:25:53
@article{88635a63-05ce-43c5-ab63-0279f9a28757,
  abstract     = {In vitro studies suggest that the G protein-coupled receptor GPR30 is a functional estrogen receptor. However, the physiological role of GPR30 in vivo is unknown, and it remains to be determined if GPR30 is an estrogen receptor also in vivo. To this end, we studied the effects of disrupting the GPR30 gene in female and male mice. Female GPR30((-/-)) mice had hyperglycemia and impaired glucose tolerance, reduced body growth, increased blood pressure, and reduced serum insulin-like growth factor-I levels. The reduced growth correlated with a proportional decrease in skeletal development. The elevated blood pressure was associated with an increased vascular resistance manifested as an increased media:lumen ratio of the resistance arteries. The hyperglycemia and impaired glucose tolerance in vivo were associated with decreased insulin expression and release in vivo and in vitro in isolated pancreatic islets. GPR30 is expressed in islets, and GPR30 deletion abolished estradiol-stimulated insulin release both in vivo in ovariectomized adult mice and in vitro in isolated islets. Our findings show that GPR30 is important for several metabolic functions in female mice including estradiol-stimulated insulin release.},
  author       = {Mårtensson, Ulrika and Salehi, S Albert and Windahl, Sara and Gomez, Maria and Swärd, Karl and Daszkiewicz-Nilsson, Joanna and Wendt, Anna and Andersson, Niklas and Hellstrand, Per and Grände, Per-Olof and Owman, Christer and Rosen, Clifford J and Adamo, Martin L and Lundquist, Ingmar and Rorsman, Patrik and Nilsson, Bengt-Olof and Ohlsson, Claes and Olde, Björn and Leeb-Lundberg, Fredrik},
  issn         = {0013-7227},
  language     = {eng},
  number       = {2},
  pages        = {687--698},
  publisher    = {Endocrine Society},
  series       = {Endocrinology},
  title        = {Deletion of the G protein-coupled Receptor GPR30 Impairs Glucose Tolerance, Reduces Bone Growth, Increases Blood Pressure, and Eliminates Estradiol-stimulated Insulin Release in Female Mice.},
  url          = {http://dx.doi.org/10.1210/en.2008-0623},
  volume       = {150},
  year         = {2009},
}