The anorectic agent, lorcaserin, disturbs estrous cyclicity and produces endometrial hyperplasia without affecting ovarian population in female rats

Life Sciences ◽  
2017 ◽  
Vol 183 ◽  
pp. 69-77 ◽  
Author(s):  
Raghda T. Abdel-Latif ◽  
Sawsan A. Zaitone ◽  
Yousra Abdel-mottaleb ◽  
Nabila N. El-Maraghy
Keyword(s):  
Endometrial Hyperplasia ◽  
Female Rats ◽  
Estrous Cyclicity ◽  
Anorectic Agent

scholarly journals Glyphosate-based herbicide enhances the uterine sensitivity to estradiol in rats

2018 ◽  
Vol 239 (2) ◽  
pp. 197-213 ◽  
Author(s):  
Marlise Guerrero Schimpf ◽  
María M Milesi ◽  
Enrique H Luque ◽  
Jorgelina Varayoud
Keyword(s):  
Cell Proliferation ◽  
Endometrial Hyperplasia ◽  
Low Dose ◽  
Saline Solution ◽  
Female Rats ◽  
Postnatal Exposure ◽  
Rat Uterus ◽  
Mrna Extraction ◽  
17Β Estradiol ◽  
Prepubertal Rats

In a previous work, we detected that postnatal exposure to a glyphosate-based herbicide (GBH) alters uterine development in prepubertal rats causing endometrial hyperplasia and increasing cell proliferation. Our goal was to determine whether exposure to low dose of a GBH during postnatal development might enhance the sensitivity of the uterus to an estrogenic treatment. Female Wistar pups were subcutaneously injected with saline solution (control) or GBH using the reference dose (2 mg/kg/day, EPA) on postnatal days (PND) 1, 3, 5 and 7. At weaning (PND21), female rats were bilaterally ovariectomized and treated with silastic capsules containing 17β-estradiol (E2, 1 mg/mL) until they were 2 months of age. On PND60, uterine samples were removed and processed for histology, immunohistochemistry and mRNA extraction to evaluate: (i) uterine morphology, (ii) uterine cell proliferation by the detection of Ki67, (iii) the expression of the estrogen receptors alpha (ESR1) and beta (ESR2) and (iv) the expression of WNT7A and CTNNB1. GBH-exposed animals showed increased luminal epithelial height and stromal nuclei density. The luminal and glandular epithelium were markedly hyperplastic in 43% of GBH-exposed animals. GBH exposure caused an increase in E2-induced cell proliferation in association with an induction of both ESR1 and ESR2. GBH treatment decreased membranous and cytoplasmic expression of CTNNB1 in luminal and glandular epithelial cells and increased WNT7A expression in the luminal epithelium. These results suggest that early postnatal exposure to a GBH enhances the sensitivity of the rat uterus to estradiol and induces histomorphological and molecular changes associated with uterine hyperplasia.

Prolonged Neonatal Exposure to Estrogen Inhibits Pulsatile LH Release and Estrous Cyclicity in Female Rats Probably Via Disruption of the Arcuate Metastin/Kisspeptin Neurons.

2008 ◽  
Vol 78 (Suppl_1) ◽  
pp. 146-146
Author(s):  
Yoko Inamoto ◽  
Tamami Homma ◽  
Yoshihisa Uenoyama ◽  
Maki Maeda ◽  
Shunji Yamada ◽  
...  
Keyword(s):  
Female Rats ◽  
Neonatal Exposure ◽  
Estrous Cyclicity ◽  
Lh Release

Amelioration of estrogen-induced endometrial hyperplasia in female rats by hemin via heme-oxygenase-1 expression, suppression of iNOS, p38 MAPK, and Ki67

2019 ◽  
Vol 97 (12) ◽  
pp. 1159-1168
Author(s):  
Fatma F. Ali ◽  
Walaa Yehia Abdelzaher ◽  
Randa Ahmed Ibrahim ◽  
Doaa Mohamed Elroby Ali
Keyword(s):  
Protein Kinase ◽  
Heme Oxygenase ◽  
Endometrial Hyperplasia ◽  
Mitogen Activated Protein Kinase ◽  
Female Rats ◽  
Interleukin 1Β ◽  
Estradiol Valerate ◽  
Control Group ◽  
Heme Oxygenase 1 ◽  
Mitogen Activated Protein

Although heme oxygenase-1 (HO-1) is part of an endogenous defense system implicated in the homeostatic response, its role in cell proliferation and tumor progression is still controversial. Endometrial hyperplasia (EH) is associated with high risk of endometrial cancer (EC). Therefore, we aimed to evaluate the effect of hemin, a HO-1 inducer, against EH. Thirty-two female rats (60–70 days old) were divided into 4 groups treated for 1 week: vehicle control group, hemin group (25 mg/kg; i.p. 3 times/week), estradiol valerate (EV) group (2 mg/kg per day, p.o.), and hemin plus EV group. Sera were obtained for reduced glutathione level. Uterine malondialdehyde, superoxide dismutase, total nitrite/nitrate, and interleukin-1β levels were estimated. HO-1 and p38 mitogen-activated protein kinase expressions were obtained in uterine tissue. Uterine histological and immunohistochemical assessment of iNOS and Ki67 were also done. Results demonstrated that upregulation of HO-1 expression in hemin plus EV rats led to amelioration of EH which was confirmed with histological examination. This was associated with significant decrease in oxidative stress parameters, p38 mitogen-activated protein kinase expression, and interleukin-1β level. Also, uterine iNOS and Ki67 expressions were markedly suppressed. In conclusion, upregulation of HO-1 expression via hemin has ameliorative effect against EH through its antioxidant, anti-inflammatory, and antiproliferative actions.

Estrous Cyclicity and Behavioral Sensitization in Female Rats Following Repeated Intravenous Cocaine Administration

1999 ◽  
Vol 64 (3) ◽  
pp. 605-610 ◽  
Author(s):  
Rosemarie M Booze ◽  
Marcie L Wood ◽  
Marian A Welch ◽  
Stepheny Berry ◽  
Charles F Mactutus
Keyword(s):  
Behavioral Sensitization ◽  
Female Rats ◽  
Cocaine Administration ◽  
Estrous Cyclicity ◽  
Intravenous Cocaine

Relation of Circulating Estradiol and Progesterone to Gonadotropin Secretion and Estrous Cyclicity in Aging Female Rats*

Endocrinology ◽  
1985 ◽  
Vol 116 (5) ◽  
pp. 1953-1959 ◽  
Author(s):  
JOHN K. H. LU ◽  
PHILIP S. LAPOLT ◽  
THOMAS E. NASS ◽  
DENNIS W. MATT ◽  
HOWARD L. JUDD
Keyword(s):  
Female Rats ◽  
Gonadotropin Secretion ◽  
Estrous Cyclicity

scholarly journals SUN-239 Effects of High-Fat Diet-Induced Obesity on Pulsatile LH Secretion and Hypothalamic KISS1 Expression in Female Rats

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Shiori Minabe ◽  
Kinuyo Iwata ◽  
Youki Watanabe ◽  
Hitoshi Ozawa
Keyword(s):  
Body Weight ◽  
High Fat Diet ◽  
Pulse Frequency ◽  
Female Rats ◽  
Standard Diet ◽  
High Fat ◽  
Estrous Cycles ◽  
Menstrual Dysfunction ◽  
Estrous Cyclicity ◽  
Lh Secretion

Abstract Female obesity is associated with menstrual dysfunction leading to anovulation and infertility. It has recently been reported obesity-induced infertility is involved in the dysfunction of a kisspeptin neuron, a key player in reproduction via direct stimulation of gonadotropin releasing hormone (GnRH) and subsequent gonadotropin release in mammalian species. Previous studies reported that obesity due to high-fat diet (HFD) for 8 months induced a disruption in estrous cyclicity, caused by a decrease in Kiss1 (coding kisspeptin) expression in the hypothalamic arcuate nucleus (ARC) in female rodents. Here we showed the effects of shorter-term (4 months) HFD on pulsatile LH secretion and hypothalamic Kiss1 expression to show pathogenic mechanism underlying obesity-induced infertility. Female Wistar-Imamichi strain rats (7 weeks old) fed on either a standard diet (10% calories from fat) or a high-fat diet (45% calories from fat) for 4 months. Estrous cyclicity and body weight were monitored regularly. All animals were implanted with a jugular catheter and collected blood samples to analyze pulsatile LH secretion, after a week of the ovariectomy with low-dose replacement estradiol to negate influence of changes in ovarian steroid levels and mimic diestrous levels of plasma estrogen. On the next day of the blood sampling, rats were perfused with 0.05 M PBS followed by 4% paraformaldehyde and their brains were collected for in situ hybridization of Kiss1 and Gnrh1. The HFD-fed rats showed progressive increases in body weight, along with hyperphagia and adipose tissue accumulation, compared with control animals. Fifty-eight percent of the HFD-fed rats exhibited irregular estrous cycles, whereas remaining HFD-fed rats showed regular cycles. Two out of 7 rats showing HFD-induced irregular estrous cycles exhibited profound suppression of the LH pulse frequency and the number of Kiss1-expressing cells in the ARC, whereas remaining HFD-fed rats showed normal LH pulses and ARC Kiss1 expressions. The number of Kiss1-expressing cells in the ARC had close positive correlation with LH pulse frequency (R2=0.6872, P<0.001) in both groups. Additionally, the number of Kiss1- or Gnrh1-expressing cells in the anteroventral periventricular nucleus or the preoptic area, were comparable between groups. Taken together, our finding reveals the possibility that irregular menstruation was also induced by changes in the kisspeptin-GnRH independent pathway during the incipient stage of obese infertility.

Effect of Nonionizing Radiation on Progesterone Treatment in Endometrial Hyperplasia: An Experimental Rat Study

2021 ◽  
pp. 1-7
Author(s):  
Mehmet Unsal ◽  
Erdem Fadiloglu ◽  
Burcin Celik ◽  
Fatih Kilic ◽  
Omer Lutfi Tapisiz
Keyword(s):  
Epithelial Cell ◽  
Endometrial Hyperplasia ◽  
Animal Experiments ◽  
Cell Length ◽  
Female Rats ◽  
Luminal Epithelial Cell ◽  
Progesterone Treatment ◽  
Nonionizing Radiation ◽  
Group B ◽  
Rat Study

<b><i>Objectives:</i></b> The aim of the study was to evaluate the negative effect of nonionizing radiation on the treatment of endometrial hyperplasia (EH) with oral progesterone. <b><i>Design:</i></b> Forty oophorectomized Wistar Albino female rats were included in this experimental rat study. <b><i>Materials and Methods:</i></b> The 4 groups were planned as follows: Group A; sham group; Group B; group receiving oral estradiol hemihydrate 4 mg/kg/day; Group C; 4 mg/kg/day oral estradiol hemihydrate followed with 1 mg/day medroxy progesterone acetate (MPA) and Group D; 4 mg/kg/day oral estradiol hemihydrate followed with 1 mg/day MPA with exposure to nonionizing radiation at 1800 mHz/3 h/day. After the experimental model, uterine horns were sampled and the preparations were evaluated for pathological parameters (glandular density, epithelial cell length, and luminal epithelial cell length) via light microscopy. Nonionizing radiation was created by a signal generator and a compatible mobile phone. <b><i>Results:</i></b> Estrogen was found to increase all parameters related to EH (<i>p</i> &#x3c; 0.05). Progesterone treatment was found to decrease parameters related to EH (Group B vs. C; luminal epithelial cell length, glandular density, and epithelial length; 11.2 vs. 13.2 μm <i>p</i> = 0.007; 32.5 vs. 35.5, <i>p</i> = 0.068; and 219.9 μm vs. 285 µm, <i>p</i> &#x3c; 0.001, respectively). Final analyses revealed reduced effectiveness of progesterone treatment in the rats exposed to nonionizing radiation (Group C vs. D); luminal epithelial cell length, glandular density, and epithelial length (11.2 μm vs. 13.5 μm, <i>p</i> = 0.179; 32.5 vs. 52, <i>p</i> &#x3c; 0.001; and 219.9 μm vs. 374.1 μm, <i>p</i> = 0.001, respectively). <b><i>Limitations:</i></b> The limitations of our study are that the results of animal experiments may not be appropriate for direct adaptation to humans and the relatively low number of rats included in the study. <b><i>Conclusion:</i></b> Nonionizing radiation reduces the effect of progesterone in patients receiving treatment for EH.

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