Deletion of the G protein-coupled receptor 30 impairs glucose tolerance, reduces bone growth, increases blood pressure, and eliminates estradiol-stimulated insulin release in female mice.
Artikel i vetenskaplig tidskrift, 2009

In vitro studies suggest that the G protein-coupled receptor (GPR) 30 is a functional estrogen receptor. However, the physiological role of GPR30 in vivo is unknown, and it remains to be determined whether 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 IGF-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 to 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.

veterinary

Animals

Glucose Tolerance Test

metabolism

Male

Mice

Pregnancy

genetics

Gene Deletion

Glucose Intolerance

Bone Development

Inbred C57BL

Islets of Langerhans

Estradiol

Knockout

Tissue Distribution

Sex Characteristics

genetics

metabolism

Mice

Female

RNA

pharmacology

Mice

Messenger

genetics

Receptors

genetics

G-Protein-Coupled

Blood Pressure

metabolism

physiology

secretion

Insulin

Författare

Ulrika E A Mårtensson

S Albert Salehi

Sara H Windahl

Göteborgs universitet

Maria F Gomez

Karl Swärd

Joanna Daszkiewicz-Nilsson

Anna Wendt

Niklas Andersson

Göteborgs universitet

Per Hellstrand

Per-Olof Grände

Christer Owman

Clifford J Rosen

Martin L Adamo

Ingmar Lundquist

Patrik Rorsman

Bengt-Olof Nilsson

Claes Ohlsson

Göteborgs universitet

Björn Olde

L M Fredrik Leeb-Lundberg

Endocrinology

1945-7170 (ISSN)

Vol. 150 2 687-98

Ämneskategorier

Endokrinologi och diabetes

DOI

10.1210/en.2008-0623

PubMed

18845638