scholarly journals Loss of Nuclear and Membrane Estrogen Receptor-α Differentially Impairs Insulin Secretion and Action in Male and Female Mice

Diabetes ◽  
2018 ◽  
Vol 68 (3) ◽  
pp. 490-501 ◽  
Author(s):  
Camille Allard ◽  
Jamie J. Morford ◽  
Beibei Xu ◽  
Benjamin Salwen ◽  
Weiwei Xu ◽  
...  
1997 ◽  
Vol 32 (3) ◽  
pp. 176-183 ◽  
Author(s):  
Scott R Wersinger ◽  
Koen Sannen ◽  
Constanza Villalba ◽  
Dennis B Lubahn ◽  
Emilie F Rissman ◽  
...  

Endocrine ◽  
2000 ◽  
Vol 12 (3) ◽  
pp. 207-213 ◽  
Author(s):  
Srikanth Yellayi ◽  
Cory Teuscher ◽  
Jeffery A. Woods ◽  
Thomas H. Welsh ◽  
Kenneth S. K. Tung ◽  
...  

2017 ◽  
Vol 38 (5) ◽  
pp. 1061-1072 ◽  
Author(s):  
Luhong Wang ◽  
Laura L. Burger ◽  
Megan L. Greenwald-Yarnell ◽  
Martin G. Myers ◽  
Suzanne M. Moenter

Author(s):  
Emmanuel Guivarc'h ◽  
Julie Favre ◽  
Anne‐Laure Guihot ◽  
Emilie Vessières ◽  
Linda Grimaud ◽  
...  

Background The cardiovascular protective effects of estrogens in premenopausal women depend mainly on estrogen receptor α (ERα). ERα activates nuclear gene transcription regulation and membrane‐initiated signaling. The latter plays a key role in estrogen‐dependent activation of endothelial NO synthase. The goal of the present work was to determine the respective roles of the 2 ERα activities in endothelial function and cardiac and kidney damage in young and old female mice with hypertension, which is a major risk factor in postmenopausal women. Methods and Results Five‐ and 18‐month‐old female mice lacking either ERα (ERα −/− ), the nuclear activating function AF2 of ERα (AF2°), or membrane‐located ERα (C451A) were treated with angiotensin II (0.5 mg/kg per day) for 1 month. Systolic blood pressure, left ventricle weight, vascular reactivity, and kidney function were then assessed. Angiotensin II increased systolic blood pressure, ventricle weight, and vascular contractility in ERα −/− and AF2° mice more than in wild‐type and C451A mice, independent of age. In both the aorta and mesenteric resistance arteries, angiotensin II and aging reduced endothelium‐dependent relaxation in all groups, but this effect was more pronounced in ERα −/− and AF2° than in the wild‐type and C451A mice. Kidney inflammation and oxidative stress, as well as blood urea and creatinine levels, were also more pronounced in old hypertensive ERα −/− and AF2° than in old hypertensive wild‐type and C451A mice. Conclusions The nuclear ERα‐AF2 dependent function attenuates angiotensin II–dependent hypertension and protects target organs in aging mice, whereas membrane ERα signaling does not seem to play a role.


2008 ◽  
Vol 199 (2) ◽  
pp. 275-286 ◽  
Author(s):  
L Lundholm ◽  
G Bryzgalova ◽  
H Gao ◽  
N Portwood ◽  
S Fält ◽  
...  

The aim of this study was to validate the role of estrogen receptor α (ERα) signaling in the regulation of glucose metabolism, and to compare the molecular events upon treatment with the ERα-selective agonist propyl pyrazole triol (PPT) or 17β-estradiol (E2) in ob/ob mice. Female ob/ob mice were treated with PPT, E2 or vehicle for 7 or 30 days. Intraperitoneal glucose and insulin tolerance tests were performed, and insulin secretion was determined from isolated islets. Glucose uptake was assayed in isolated skeletal muscle and adipocytes. Gene expression profiling in the liver was performed using Affymetrix microarrays, and the expression of selected genes was studied by real-time PCR analysis. PPT and E2 treatment improved glucose tolerance and insulin sensitivity. Fasting blood glucose levels decreased after 30 days of PPT and E2 treatment. However, PPT and E2 had no effect on insulin secretion from isolated islets. Basal and insulin-stimulated glucose uptake in skeletal muscle and adipose tissue were similar in PPT and vehicle-treated ob/ob mice. Hepatic lipid content was decreased after E2 treatment. In the liver, treatment with E2 and PPT increased and decreased the respective expression levels of the transcription factor signal transducer and activator of transcription 3, and of glucose-6-phosphatase. In summary, our data demonstrate that PPT exerts anti-diabetic effects, and these effects are mediated via ERα.


2000 ◽  
Vol 62 (2) ◽  
pp. 310-317 ◽  
Author(s):  
Wendy N. Jefferson ◽  
John F. Couse ◽  
Elizabeth Padilla Banks ◽  
Kenneth S. Korach ◽  
Retha R. Newbold

2011 ◽  
Vol 36 (7) ◽  
pp. 981-995 ◽  
Author(s):  
Amy E. Clipperton-Allen ◽  
Anne Almey ◽  
Ashley Melichercik ◽  
Craig P. Allen ◽  
Elena Choleris

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