Comparative effects of tamoxifen and angiotensin II type-1 receptor antagonist therapy on the hemodynamic profile of the ovariectomized female rat

2003 ◽  
Vol 81 (9) ◽  
pp. 915-919 ◽  
Author(s):  
My-Lan Pham-Dang ◽  
Robert Clement ◽  
Isabelle Mercier ◽  
Angelino Calderone
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Angiotensin Ii ◽  
Receptor Antagonist ◽  
Body Weight Gain ◽  
Left Ventricular ◽  
Female Rat ◽  
Ovx Rats ◽  
Hemodynamic Profile

Hormonal replacement therapy (HRT) has failed to provide a cardioprotective action in postmenopausal women, and thus alternative pharmacological approaches are required. The present study examined the therapeutic potential of the partial estrogen receptor agonist tamoxifen and the angiotensin II type-1 receptor antagonist irbesartan on the hemodynamic profile of ovariectomized (OVX) female Sprague–Dawley rats (9–11 weeks). Three weeks following ovariectomy, uterine atrophy was evident and body weight was increased as compared with sham-operated animals. Left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), and mean arterial pressure (MAP) were significantly increased in the OVX rats as compared with sham rats. One week following ovariectomy, rats were treated with either tamoxifen (10 mg kg–1 day–1) or irbesartan (40 mg kg–1 day–1) for a period of 2 weeks. The administration of tamoxifen to OVX rats partially reversed uterine atrophy and prevented body weight gain, albeit body weight remained significantly lower than in sham-operated animals. LVSP and LVEDP were normalized in the tamoxifen-treated OVX rats, whereas MAP remained elevated. Irbesartan partially reduced the body weight gain of the OVX rats and did not influence uterine atrophy. LVSP and MAP were normalized in irbesartan-treated OVX rats, whereas LVEDP remained elevated. These data demonstrate that irbesartan rather than tamoxifen was efficacious in normalizing MAP in the OVX rats without a secondary effect on the uterus.Key words: ovariectomy, hemodynamics, tamoxifen, AT1 receptor antagonists.

Stimulation of food intake and weight gain in mature female rats by bovine prolactin and bovine growth hormone

1993 ◽  
Vol 264 (6) ◽  
pp. E986-E992 ◽  
Author(s):  
J. C. Byatt ◽  
N. R. Staten ◽  
W. J. Salsgiver ◽  
J. G. Kostelc ◽  
R. J. Collier
Keyword(s):  
Growth Hormone ◽  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
Body Weight Gain ◽  
Mature Female ◽  
Female Rats ◽  
Bovine Growth Hormone ◽  
Female Rat ◽  
Moisture Percentage

Recombinant bovine prolactin (rbPRL) or bovine growth hormone (rbGH) was administered to mature female rats (10/treatment group) by daily subcutaneous injection for 10 days. Doses ranged from 7 to 5,000 micrograms/day (0.03-24 mg/kg body wt). Both rbPRL and rbGH increased body weight gain and food intake, but these parameters were increased at lower doses of rbPRL (7-63 micrograms/day) than rbGH (> 190 micrograms/day). Weight gain and food intake were maximally stimulated by 190 micrograms/day rbPRL, whereas maximal increased weight gain was obtained with the highest dose of rbGH (5,000 micrograms/day). Total carcass protein was increased by both hormones; however, protein as a percentage of body weight was unchanged. Similarly, neither rbPRL nor rbGH changed the percentage of carcass moisture. Percentage of body fat was increased by rbPRL but was decreased by rbGH. Weight of the gastrointestinal tract and kidneys was increased by both hormones, but increases were in proportion to body weight gain. These data confirm that ungulate prolactin is a hyperphagic agent in the female rat. In addition, they suggest that, while prolactin stimulates growth in mature female rats, this growth is probably not via a somatogenic mechanism.

Effect of central angiotensin II on body weight gain in young rats

2003 ◽  
Vol 959 (1) ◽  
pp. 20-28 ◽  
Author(s):  
James P Porter ◽  
Jared M Anderson ◽  
Reid J Robison ◽  
Adam C Phillips
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Angiotensin Ii ◽  
Body Weight Gain ◽  
Young Rats

scholarly journals Deletion of miRNA-22 Induces Cardiac Hypertrophy in Females but Attenuates Obesogenic Diet-Mediated Metabolic Disorders

2020 ◽  
Vol 54 (6) ◽  
pp. 1199-1217
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Cardiac Hypertrophy ◽  
Mrna Expression ◽  
Metabolic Disorders ◽  
Body Weight Gain ◽  
Expression Profiles ◽  
Left Ventricular ◽  
Sequencing Analysis ◽  
Obesogenic Diet

Background/Aims: Obesity is a risk factor associated with cardiometabolic complications. Recently, we reported that miRNA-22 deletion attenuated high-fat diet-induced adiposity and prevented dyslipidemia without affecting cardiac hypertrophy in male mice. In this study, we examined the impact of miRNA-22 in obesogenic diet-induced cardiovascular and metabolic disorders in females. Methods: Wild type (WT) and miRNA-22 knockout (miRNA-22 KO) females were fed a control or an obesogenic diet. Body weight gain, adiposity, glucose tolerance, insulin tolerance, and plasma levels of total cholesterol and triglycerides were measured. Cardiac and white adipose tissue remodeling was assessed by histological analyses. Echocardiography was used to evaluate cardiac function and morphology. RNA-sequencing analysis was employed to characterize mRNA expression profiles in female hearts. Results: Loss of miRNA-22 attenuated body weight gain, adiposity, and prevented obesogenic diet-induced insulin resistance and dyslipidemia in females. WT obese females developed cardiac hypertrophy. Interestingly, miRNA-22 KO females displayed cardiac hypertrophy without left ventricular dysfunction and myocardial fibrosis. Both miRNA-22 deletion and obesogenic diet changed mRNA expression profiles in female hearts. Enrichment analysis revealed that genes associated with regulation of the force of heart contraction, protein folding and fatty acid oxidation were enriched in hearts of WT obese females. In addition, genes related to thyroid hormone responses, heart growth and PI3K signaling were enriched in hearts of miRNA-22 KO females. Interestingly, miRNA-22 KO obese females exhibited reduced mRNA levels of Yap1, Egfr and Tgfbr1 compared to their respective controls. Conclusion: This study reveals that miRNA-22 deletion induces cardiac hypertrophy in females without affecting myocardial function. In addition, our findings suggest miRNA-22 as a potential therapeutic target to treat obesity-related metabolic disorders in females.

Food intake inhibition and reduction in body weight gain in rats treated with GI264879A, a non-selective NPY-Y1 receptor antagonist

Peptides ◽  
2001 ◽  
Vol 22 (3) ◽  
pp. 483-491 ◽  
Author(s):  
A.J Danielsa ◽  
W.T Chance ◽  
M.K Grizzle ◽  
D Heyer ◽  
J.E Matthews
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
Receptor Antagonist ◽  
Body Weight Gain ◽  
Y1 Receptor

scholarly journals Angiotensin II Type 1-Receptor Antagonist Candesartan Cilexitil Prevents Left Ventricular Dysfunction in Myocardial Infarcted Rats

1998 ◽  
Vol 78 (1) ◽  
pp. 45-54 ◽  
Author(s):  
Hanatani Akihisa ◽  
Yoshiyama Minoru ◽  
Takeuchi Kazuhide ◽  
Kim Shokei ◽  
Nakayama Koji ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Receptor Antagonist ◽  
Left Ventricular Dysfunction ◽  
Ventricular Dysfunction ◽  
Left Ventricular

scholarly journals Estrogen suppresses adipogenesis by inhibiting S100A16 expression

2014 ◽  
Vol 52 (3) ◽  
pp. 235-244 ◽  
Author(s):  
Rihua Zhang ◽  
Dongming Su ◽  
Weidong Zhu ◽  
Qiong Huang ◽  
Menglan Liu ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Molecular Mechanisms ◽  
Body Weight Gain ◽  
Abdominal Fat ◽  
Luciferase Assay ◽  
Marker Genes ◽  
Embryonic Fibroblasts ◽  
Fat Accumulation ◽  
Ovx Rats

The aim of this study is to determine the effects of E2 on metabolic syndrome and the molecular mechanisms involving S100A16. Ovariectomized (OVX) rat models and mouse embryonic fibroblasts cell models were used. E2 loss in OVX rats induced body weight gain and central abdominal fat accumulation, which were ameliorated by E2 treatment under chow and high-fat diet (HFD) conditions. E2 decreased the expression of the adipocyte marker genes PPARγ, aP2, C/EBPα, and S100A16. E2 inhibited adipogenesis. Overexpression of S100A16 reversed the E2-induced adipogenesis effect. A luciferase assay showed that E2 inhibited the expression of S100A16. E2 treatment decreased body weight gain and central abdominal fat accumulation under both chow and HFD conditions. Also, E2 suppressed adipogenesis by inhibiting S100A16 expression.

scholarly journals Gastric inhibitory polypeptide receptor antagonist, SKL-14959, suppressed body weight gain on diet-induced obesity mice

2018 ◽  
Vol 4 (2) ◽  
pp. 194-203 ◽  
Author(s):  
T. Nakamura ◽  
H. Tanimoto ◽  
Y. Mizuno ◽  
M. Okamoto ◽  
M. Takeuchi ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Receptor Antagonist ◽  
Body Weight Gain ◽  
Gastric Inhibitory Polypeptide ◽  
Diet Induced Obesity
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