Estrogen replacement increases β-arrestin2 expression in cardiac tissues in ovariectomized rats

2015 ◽  
Vol 36 (6) ◽  
pp. 634
Author(s):  
Fan HAO ◽  
Xing TAN ◽  
Wei-zhong WANG ◽  
Ming-juan XU
Keyword(s):  
Ovariectomized Rats ◽  
Estrogen Replacement ◽  
Cardiac Tissues

Energy balance in ovariectomized rats with and without estrogen replacement

1980 ◽  
Vol 238 (5) ◽  
pp. R400-R405 ◽  
Author(s):  
M. L. Laudenslager ◽  
C. W. Wilkinson ◽  
H. J. Carlisle ◽  
H. T. Hammel
Keyword(s):  
Energy Balance ◽  
Heat Loss ◽  
Body Mass ◽  
Heat Production ◽  
Hormone Treatment ◽  
Ovariectomized Rats ◽  
Dark Phase ◽  
Evaporative Heat Loss ◽  
Estrogen Replacement ◽  
Dry Heat

The effect of estrogen replacement on several parameters of energy balance was investigated in ovariectomized rats tested during the dark phase of their diurnal cycle. Estrogen replacement, either as 17 beta-estradiol or beta-estradiol-3-benzoate via subcutaneous Silastic capsules, was associated with elevated rates of heat production and dry heat loss relative to untreated ovariectomized controls. Estrogen treatment reduced body mass and retarded fur growth. The effects of estrogen replacement on heat production and dry heat loss could not be attributed to these differences in body mass and fur growth or locomotor activity. Estrogen replacement had no effect on rate of evaporative heat loss. If estrogen replacement was delayed 75 days following ovariectomy, the increase in heat production and dry heat loss was not observed. There was no effect of the hormone treatment on rectal temperature. It was concluded that either heat production was elevated, with dry heat loss increased to compensate for the additional thermal load, or dry heat loss was accelerated with heat production elevated in compensation.

Activin βA subunit, follistatin and follistatin-like 3 are expressed in the endometrium of ovariectomized rats and regulated by estrogen replacement

2008 ◽  
Vol 39 (5) ◽  
pp. 535-541 ◽  
Author(s):  
Márcia C. Ferreira ◽  
Inês K. D. Cavallo ◽  
Pasquale Florio ◽  
Felice Petraglia ◽  
Fernando M. Reis
Keyword(s):  
Ovariectomized Rats ◽  
Estrogen Replacement

Effects of resistance training and estrogen replacement on adipose tissue inflammation in ovariectomized rats

2017 ◽  
Vol 42 (6) ◽  
pp. 605-612 ◽  
Author(s):  
Maria Fernanda Cury Rodrigues ◽  
Fabiano Candido Ferreira ◽  
Natália Santanielo Silva-Magosso ◽  
Marina Rodrigues Barbosa ◽  
Markus Vinicius Campos Souza ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Resistance Training ◽  
Ovariectomized Rats ◽  
Low Grade ◽  
Estrogen Replacement ◽  
Expression Levels ◽  
Inflammatory Status ◽  
Ovx Rats ◽  
Tnf Α ◽  
Gene And Protein Expression

Estrogen deficiency is directly related to central obesity and low-grade inflammation. Hormonal replacement and exercise training are both able to decrease fat accumulation and inflammation in postmenopausal women. However, the efficiency of resistance training (RT) and estrogen replacement (ER) in minimizing adiposity and inflammation in the visceral adipose tissue (VAT) of ovariectomized (OVX) rats has not yet been elucidated. In this study, Sprague–Dawley rats were divided into the following 6 groups: sham-operated sedentary (Sham-Sed), OVX-Sed, Sham-RT, OVX-RT, OVX-Sed-ER, and OVX-RT-ER groups. ER was performed by implanting silastic capsules containing 17β-estradiol. For RT, the animals were required to climb a 1.1-m vertical ladder with conical flasks containing weights attached to their tails for 12 weeks. Histological analyses were used to evaluate morphological changes. Gene expression levels were determined by quantitative real-time reverse transcriptase polymerase chain reaction, and protein concentrations were determined using Multiplex/Luminex assays. Ovariectomy increased the body mass (BM), adipocyte area, and inflammation in the VAT, the latter of which was indicated by reduced interleukin-10 (48%) and increased tumor necrosis factor (TNF)-α concentration (∼3%). RT efficiently decreased BM, adipocyte area, and inflammation in the OVX groups. The combination of RT and ER decreased BM (19%) and the TNF-α concentration (18%) and increased the gene and protein expression levels of adiponectin (173% and 18%). These results indicate that RT and the combination of RT and ER are efficient strategies for reducing the BM and improving the inflammatory status of OVX rats.

scholarly journals Estrogen Inhibits Colon Polyp Formation by Reducing Angiogenesis in a Carcinogen-Induced Rat Model

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Jia Yang ◽  
Li-juan Xiong ◽  
Fei Xu ◽  
Xiang Zhao ◽  
Bo Liu ◽  
...  
Keyword(s):  
Rat Model ◽  
Colon Polyp ◽  
Ovariectomized Rats ◽  
Nuclear Antigen ◽  
Control Group ◽  
Colon Polyps ◽  
Estrogen Replacement ◽  
Polyp Formation ◽  
Ovx Rats ◽  
Proliferating Cell

Objective.To study the effects of estrogen on colon polyp formation, proliferation, and angiogenesis on a rat model of colon cancer induced by dimethylhydrazine (DMH).Methods.Thirty-six female ovariectomized (OVX) rats were randomly divided into 3 groups: (I) control group (administrated with vehicles weekly), (II) DMH group (administrated with DMH weekly), and (III) DMH + E2group (administrated with DMH and 17β-estradiol weekly). The incidence, volumes, and multiplicity of colon polyps in each group were evaluated. The microvessel density (MVD), the expressions of Proliferating Cell Nuclear Antigen (PCNA), and the expressions of HIF-1αand VEGF in polyps were detected in each group.Results.Estrogen reduced the multiplicity, volumes, and the PCNA expressions of DMH-induced colon polyps. The MVD in DMH + E2group was significantly lower than that in DMH group. Estrogen treatment decreased the HIF-1αand VEGF expressions at both mRNA and protein level.Conclusion.Estrogen replacement was protective for ovariectomized rats from DMH-induced carcinogenesis, and one of the mechanisms for this was due to estrogen’s inhibitive effects on blood vessel formation by downregulating VEGF and HIF-1αexpressions.

scholarly journals Effects of estrogen replacement on stress-induced cardiovascular responses via renin-angiotensin system in ovariectomized rats

2016 ◽  
Vol 311 (5) ◽  
pp. R898-R905 ◽  
Author(s):  
Shoko Tazumi ◽  
Naoko Yokota ◽  
Mizuho Kawakami ◽  
Sayo Omoto ◽  
Akira Takamata ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Psychological Stress ◽  
Pressor Response ◽  
Renin Angiotensin System ◽  
Cardiovascular Responses ◽  
Ovariectomized Rats ◽  
Separate Experiment ◽  
Estrogen Replacement ◽  
Angiotensin System ◽  
Renin Angiotensin

The purpose of this study was to determine whether chronic estrogen replacement in ovariectomized rats inhibits the pressor response to psychological stress by attenuating the activation of the renin-angiotensin system. Female Wistar rats aged 9 wk were ovariectomized. After 4 wk, the rats were randomly assigned to be implanted subcutaneously with pellets containing either 17β-estradiol (E2) or placebo (Pla). After 4 wk of treatment, the rats underwent cage-switch stress and, in a separate experiment, a subset received an infusion of angiotensin II. The cage-switch stress rapidly elevated blood pressure (BP) and heart rate (HR) as measured by radiotelemetry in both groups. However, the BP and HR responses to the stress were significantly attenuated in the E2 group compared with the Pla group. An angiotensin II type 1 receptor blocker, losartan, given in drinking water, abolished the difference in the pressor response to stress between the two groups. Moreover, the stress-induced elevation in plasma renin activity and angiotensin II concentration was significant in the Pla group, but not in the E2 group. In addition, the expression of renin mRNA in the kidney was lower in the E2 group relative to the Pla group. Finally, we found that intravenous angiotensin II infusion increased BP and decreased HR to a similar degree in both groups. These results suggest that the inhibitory effects of estrogen on psychological stress-induced activation of the renin-angiotensin system could be at least partially responsible for the suppression of the pressor responses to psychological stress seen in estrogen-replaced ovariectomized rats.

scholarly journals Effect of estrogen replacement on liver function in ovariectomized rats.

1991 ◽  
Vol 16 (3) ◽  
pp. 87-100 ◽  
Author(s):  
Yusuke NAGAE ◽  
Masaki MIYAMOTO ◽  
Hajime MIYAMOTO
Keyword(s):  
Liver Function ◽  
Ovariectomized Rats ◽  
Estrogen Replacement

scholarly journals Estrogen replacement attenuates stress-induced pressor responses through vasorelaxation via β2-adrenoceptors in peripheral arteries of ovariectomized rats

2018 ◽  
Vol 314 (2) ◽  
pp. H213-H223 ◽  
Author(s):  
Shoko Tazumi ◽  
Sayo Omoto ◽  
Yu Nagatomo ◽  
Mariko Kawahara ◽  
Naoko Yokota-Nakagi ◽  
...  
Keyword(s):  
Mesenteric Artery ◽  
Pressor Response ◽  
Mrna Level ◽  
Treated Group ◽  
Inhibitory Effect ◽  
Ovariectomized Rats ◽  
Peripheral Arteries ◽  
Estrogen Replacement ◽  
Depressor Response ◽  
Pressor Responses

We examined whether chronic estrogen replacement has an inhibitory effect on stress-induced pressor responses via activation of β2-adrenoceptor (AR) in peripheral arteries of ovariectomized rats. Female Wistar rats aged 9 wk were ovariectomized. After 4 wk, pellets containing either 17β-estradiol (E2) or placebo (Pla) were subcutaneously implanted into the rats. After 4 wk of treatment, rats underwent cage-switch stress, and, in a separate experiment, a subset received an infusion of isoproterenol (ISO) with or without pretreatment with the β1-AR blocker atenolol or the β2-AR blocker butoxamine. In addition, the isolated mesenteric artery was used to assess the concentration-related relaxing responses to ISO and the β1- or β2-AR mRNA level. The cage-switch stress-induced pressor response was significantly attenuated in the E2-treated group compared with the Pla-treated group. Pretreatment with atenolol reduced blood pressure responses in both groups. However, butoxamine enhanced the pressor response only in the E2-treated group, resulting in no difference between the two groups. In addition, the intravenous ISO-induced depressor response was significantly enhanced in the E2-treated group compared with the Pla-treated group. Furthermore, the difference in the depressor response was abolished by pretreatment with butoxamine but not by atenolol. In the isolated mesenteric artery, butoxamine caused a rightward shift in ISO-induced concentration-related relaxation in the E2-treated group. The β2-AR mRNA level in the mesenteric artery was higher in the E2-treated group than in the Pla-treated group. These results suggest that estrogen replacement attenuated the stress-induced pressor response probably by suppressing vasoconstriction via activation of β2-ARs in peripheral arteries of ovariectomized rats. NEW & NOTEWORTHY In this study, we show, for the first time, that estrogen replacement has an inhibitory effect on the psychological stress-induced pressor response through vasorelaxation via β2-adrenoceptors, probably due to overexpression of β2-adrenoceptor mRNA, in peripheral arteries of ovariectomized rats.

scholarly journals Estrogen replacement enhances insulin-induced AS160 activation and improves insulin sensitivity in ovariectomized rats

2018 ◽  
Vol 315 (6) ◽  
pp. E1296-E1304 ◽  
Author(s):  
Mizuho Kawakami ◽  
Naoko Yokota-Nakagi ◽  
Masami Uji ◽  
Ken-ichi Yoshida ◽  
Shoko Tazumi ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Glucose Transporter ◽  
Glycogen Synthase ◽  
Ovariectomized Rats ◽  
Whole Body ◽  
Similar Degree ◽  
Mrna Levels ◽  
Estrogen Replacement ◽  
Intravenous Glucose

Menopause predisposes women to impaired glucose metabolism, but the role of estrogen remains unclear. In this study, we examined the effects of chronic estrogen replacement on whole body insulin sensitivity and insulin signaling in ovariectomized rats. Female Wistar rats aged 9 wk were ovariectomized under anesthesia. After 4 wk, pellets containing either 17β-estradiol (E2) or placebo (Pla) were subcutaneously implanted in the rats. After 4 wk of treatment, the intra-abdominal fat accumulation was greater in the Pla group than that in the E2 group. Hyperinsulinemic-euglycemic clamp analysis and intravenous glucose tolerance test revealed that insulin sensitivity was significantly lower in the Pla group than in the E2 group. In addition, Western blotting showed that in vivo insulin stimulation increased protein kinase B (Akt) phosphorylation to a similar degree in the gastrocnemius and liver of both groups, but phosphorylated Akt2 Ser474 was enhanced in the muscle of the E2 group compared with the Pla group. Moreover, insulin-stimulated phosphorylation of Akt substrate of 160 kDa (AS160) Thr642 was observed only in the E2 group, resulting in the difference between the two groups. Additionally, AS160 protein and mRNA levels were higher in muscle of the E2 group than the Pla group. In contrast, E2 replacement had no effect on glucose transporter 4 protein levels in muscle and glycogen synthase kinase-3β in muscle and liver. These results suggest that estrogen replacement improves insulin sensitivity by activating the Akt2/AS160 pathway in the insulin-stimulated muscle of ovariectomized rats.

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