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ludc web

Anna Wendt

Assistant researcher

ludc web

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.

Author

  • Ulrika Mårtensson
  • S Albert Salehi
  • Sara Windahl
  • Maria Gomez
  • Karl Swärd
  • Joanna Daszkiewicz-Nilsson
  • Anna Wendt
  • Niklas Andersson
  • Per Hellstrand
  • Per-Olof Grände
  • Christer Owman
  • Clifford J Rosen
  • Martin L Adamo
  • Ingmar Lundquist
  • Patrik Rorsman
  • Bengt-Olof Nilsson
  • Claes Ohlsson
  • Björn Olde
  • Fredrik Leeb-Lundberg

Summary, in English

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.

Department/s

  • Drug Target Discovery
  • Vascular Physiology
  • Diabetes - Islet Cell Exocytosis
  • Section II
  • Cardiology

Publishing year

2009

Language

English

Pages

687-698

Publication/Series

Endocrinology

Volume

150

Issue

2

Document type

Journal article

Publisher

Oxford University Press

Topic

  • Endocrinology and Diabetes

Status

Published

Research group

  • Drug Target Discovery
  • Vascular Physiology
  • Diabetes - Islet Cell Exocytosis

ISBN/ISSN/Other

  • ISSN: 0013-7227