• Journal of Microbiology and Biotechnology
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• v.27 no.12
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• pp.2228-2236
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• 2017

During menopausal transition, the imbalance of estrogen causes body weight gain. Although gut microbiome dysbiosis has been reported in postmenopausal obesity, it is not clear whether there is any difference in the microbiome profile between dietary-induced obesity and postmenopausal obesity. Therefore, in this study, we analyzed intestinal samples from ovariectomized mice and compared them with those of mice with high-fat diet-induced obesity. To further evaluate the presence of menopause-specific bacteria-gene interactions, we also analyzed the liver transcriptome. Investigation of the 16S rRNA V3-V4 region amplicon sequence profile revealed that menopausal obesity and dietary obesity resulted in similar gut microbiome structures. However, Bifidobacterium animalis was exclusively observed in the ovariectomized mice, which indicated that menopausal obesity resulted in a different intestinal microbiome than dietary obesity. Additionally, several bacterial taxa (Dorea species, Akkermansia muciniphila, and Desulfovibrio species) were found when the ovariectomized mice were treated with a high-fat diet. A significant correlation between the above-mentioned menopause-specific bacteria and the genes for female hormone metabolism was also observed, suggesting the possibility of bacteria-gene interactions in menopausal obesity. Our findings revealed the characteristics of the intestinal microbiome in menopausal obesity in the mouse model, which is very similar to the dietary obesity microbiome but having its own diagnostic bacteria.

• Biomedical Science Letters
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• v.13 no.2
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• pp.99-104
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• 2007

To determine whether 17$\beta$-estradiol induces the morphological changes in adipose and liver tissues, we measured the effects of 17$\beta$-estradiol on adipose tissue mass, adipocyte histology and hepatic lipid accumulation in female ovariectomized (OVX) C57BL/6J mice. Compared to vehicle-treated control mice, 17$\beta$-estradiol-treated mice decreased adipose tissue mass and the size of adipocytes, and concomitantly increased the number of adipocytes in a dose-dependent manner. In addition, the administration of 17$\beta$-estradiol resulted in reduced hepatic lipid accumulation in a dose-dependent manner. These results suggest that estrogen may regulate adipocyte development and lipid metabolism in female OVX C57BL/6J mice.

• Biomedical Science Letters
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• v.15 no.3
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• pp.171-177
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• 2009

This study investigated whether increased adiposity is prevented by estrogen replacement in female ovariectomized (OVX) C57BL/6J mice, an animal model of human menopause and whether these metabolic changes reflect the inhibitory action of estrogen on peroxisome proliferator-activated receptor $\gamma$ ($PPAR{\gamma}$)-regulated gene expression. Treatment of $17{\beta}$-estradiol for the last one week of the experiment decreased high fat diet-induced body weight gain and white adipose tissue mass compared to OVX control mice. Histological analysis showed that administration of $17{\beta}$-estradiol to mice decreased the size of adipocytes in parametrial adipose tissue versus OVX control mice. In addition, $17{\beta}$-estradiol reduced the adipose expression of $PPAR{\gamma}$ as well as $PPAR{\gamma}$ target genes such as adipocyte fatty acid binding protein and tumor necrosis factor $\alpha$. These results suggest that $17{\beta}$-estradiol may inhibit adiposity through reducing the $PPAR{\gamma}$ activities in female OVX mice.

• Biomedical Science Letters
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• v.14 no.3
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• pp.131-137
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• 2008

Adipogenesis is a complex sequence of events that culminates in the differentiation of fibroblast-like preadipocytes into specialized lipid-filled adipocytes and also involves a cascade of expression of many transcription factors such as peroxisome proliferator-activated receptor ${\gamma}(PPAR{\gamma})$ and CCAAT/enhancer-binding proteins (C/EBPs). $PPAR{\gamma}$ and C/EBPs transcriptionally transactivate adipocyte specific genes, including fatty acid transport protein (FAT/CD36) and leptin. To determine whether $17{\beta}$-estradiol modulates $C/EBP{\alpha}$ actions on adipogenesis in high fat diet-fed female ovariectomized (OVX) C57BL/6 mice, mice were treated with $17{\beta}$-estradiol for 7 days and the effects of $17{\beta}$-estradiol on adipose tissue mass and expression of adipocyte specific gene as well as $C/EBP{\alpha}$ were measured. Compared to vehicle-treated OVX control mice, OVX mice treated with $17{\beta}$-estradiol for 7 days had lower adipose tissue weights that were similar to weights in high fat diet-fed sham-operated (Sham) mice. OVX mice showed the increased expression of $C/EBP{\alpha}$ mRNA compared with Sham mice. However, $17{\beta}$-estradiol treatment in OVX mice inhibited OVX induced-$C/EBP{\alpha}$ activation, indicating that $17{\beta}$-estradiol may act as an inhibitor of $C/EBP{\alpha}$ action. Moreover, $17{\beta}$-estradiol decreased mRNA levels of adipocyte marker genes, such as lipoprotein lipase, FAT/CD36 and leptin, to levels in Sham mice. These results suggest that down-regulation of adipogenesis by $17{\beta}$-estradiol may be due to reduced adipose $C/EBP{\alpha}$ activities in female OVX C57BL/6 mice.

• Journal of the Korean Applied Science and Technology
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• v.40 no.2
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• pp.244-257
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• 2023

This study investigated the effects of exercise on genistein-induced adipose tissue reduction and anti-inflammation of adipose tissue in ovariectomized mice fed a high-fat diet. Compared to mice fed a high-fat diet (C), both genistein (G) or exercise only (Ex) not only decreased adipose tissue weight and adipocyte size, but also glucose and free fatty acid levels in serum, which were more effectively reduced when genistein and exercise were treated simultaneously (G/Ex). The expression of lipogenesis and inflammatory cytokine genes of both G and Ex in adipose tissue was decreased compared to C. In particular, the decrease of these genes expression in G/Ex was more effective than each treatment alone. Thus, this study revealed that simultaneous treatment of genistein and exercise resulted in more effective improvement of obesity and adipose tissue inflammation than genistein single treatment in ovariectomized mice fed a high-fat diet, and it is a result of positive regulation of lipogenesis genes. This study suggests that the exercise has a beneficial effect on anti-obesity and adipose tissue anti-inflammation of genistein.

• Journal of the Korean Applied Science and Technology
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• v.34 no.3
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• pp.427-435
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• 2017

To investigate whether genistein regulates menopause-induced obesity, it was studied the effects of genistein on anti-obesity effects in female ovariectomized (OVX) mice, an animal model of postmenopausal women. 7-week-old female mice (C57BL/6J) were randomly divided into three groups. All the animals received a high fat diet or a high fat diet supplemented with genistein for 8 weeks and variables and determinants of obesity were measured. The OVX mice had significantly higher body weight and adipose tissue mass than sham mice. However, genistein supplementation reduced body weight, adipose tissue mass, and adipocyte size of OVX mice. The OVX mice treated with genistein had significantly lower levels of serum triglycerides and total cholesterol than the vehicle-treated OVX mice. Lipid accumulation in liver was also markedly decreased by genistein in OVX mice. The results suggest that genistein can effectively prevent adiposity, adipocyte phertrophy, and llipid disorders caused by ovariectomy. Moreover, this study may contribute to the alleviation of metabolic syndrome, including obesity and hyerlipidemia in postmenopausal women.

• Korean Journal of Acupuncture
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• v.25 no.1
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• pp.165-196
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• 2008

Objective : The purpose of this study is to observe the effects of herbal-acupuncture with Acanthopanacis cortex extract (AC-HA) at KI10 (Eumgok) on osteoporosis in ovariectomized (OVX) ddy mice. Methods : We carried out several experimental items to analyze the changes in body weight, uterine weight, uterus index, tibial length, the ash bone weight, tibial BMD, serum ALP, serum creatinine, serum osteocalcin, serum Ca, and the levels of Ca, P, Ca/P ratio in tibia, and we performed histological and histomorphological analysis as well. Results : Tibial BMD was significantly decreased by OVX, while significantly increased by AC-HA at KI10. Serum creatinine level was significantly increased by OVX, while significantly decreased by AC-HA at KI10. Serum osteocalcin level was significantly increased by OVX, while significantly decreased by AC-HA at KI10. Tibial TBV(trabecular bone volume) was significantly decreased by OVX, while significantly increased by AC-HA at KI10. AC-HA at KI10 significantly suppressed the OVX-induced increase of GPL(growth plate length) of tibia in mice. Conclusion : These results suggest that AC-HA at KI10 has a therapeutic effect on osteoporosis in OVX mice.

• The Korean Journal of Zoology
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• v.8 no.2
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• pp.23-27
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• 1965

The present study is an analysis of some alterations occurring in the population of folliclesin the ovary treated with the gonadotrophins in intact and unilaterally ovariectomized mice. the differences between the findings inthe intact and semispayed animals and those in gonadotrophintreated intact and semispayed animals were disucssed. 1) When mice were semispayed at the stage of diestrus, the remaining ovary showed an increase of secondary follicles in number, while a decrease of atretic folicles, compared with those in intact animals. 2) After injection of PMS and HCG following semispaying at the diestrus stage, the remaining ovary contained larger number of secondary follicles and corpora lutea than those in semispayed animals with no treatment , while showed smaller number of atretic follicles. 3) It is sure that follicular development is remarkably accelerated in the intact mice treated with PMS and HCG. 4) The effect of PMS and HCG on the follicular development was gradually decreased with time in the intact and semispayed animals afte rexogenous hormone therapy. 5) It is believed in the experiment that a decrease of follicular atresia in number and an increase of secondary follicles may be responsible for compensatory reaction after semispaying.

• Journal of Convergence Korean Medicine
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• v.5 no.2
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• pp.23-27
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• 2023

Objectives: The purpose of this study was to investigate the ameliorative effects of the Epimedium koreanum Nakai (EK) on menopausal obesity in mice. Methods: To induce the menopausal obesity, female C57BL/6J mice were ovariectomized and fed with high fat diet for 12 weeks. 17β-estradiol was injected as a positive control and the extract of EK was orally administered 5 times per week for 6 weeks. Body weight, uterine weight and visceral fat weight were measured. The size of the adipocyte in visceral fat tissues was estimated by Hematoxylin and eosin staining. Fasting glucose level was estimated in serum. Results: Body weight and visceral fat weight were significantly decreased by EK treatment, while the uterine weight/body weight was increased in high fat diet-fed ovariectomized mice. The diameter of adipocyte in the visceral fat tissues was markedly reduced in EK-treated menopausal obese mice. In addition, the fasting blood glucose level was inhibited by oral EK administration. Conclusion: In conclusion, these results showed that EK has ameliorative effects on overweight after menopause. EK could be one of the alternative therapy for treating menopausal obesity.

• Journal of Ginseng Research
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• v.44 no.3
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• pp.519-526
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• 2020

Background: Bisphenol A (BPA), known as an endocrine disruptor, is widely used in the world. BPA is reported to cause inflammation-related diseases. Korean Red Ginseng (KRG) has been used safely in human for a long time for the treatment of diverse diseases. KRG has been reported of its mitigating effect on menopausal symptoms and suppress adipose inflammation. Here, we investigate the protective effect of orally administered KRG on the impacts of BPA in the liver and uterus of menopausal mice model. Methods: The transcriptome analysis for the effects of BPA on mice liver was evaluated by Gene Expression Omnibus (GEO) database-based data (GSE26728). In vivo assay to evaluate the protective effect of KRG on BPA impact in ovariectomized (OVX) mice were designed and analyzed by RNA sequencing. Results: We first demonstrated that BPA induced 12 kinds of gene set in the liver of normal mice. The administration of BPA and KRG did not change body, liver, and uterine weight in OVX mice. KRG downregulated BPA-induced inflammatory response and chemotaxis-related gene expression. Several gene set enrichment analysis (GSEA)-derived inflammatory response genes increased by BPA were inhibited by KRG in OVX mice. Conclusion: Our data suggest that BPA has commonly influenced inflammatory response effects on both normal and OVX mice. KRG protects against BPA impact of inflammatory response and chemotaxis in OVX mouse models. Our comparative analysis will provide new insight into the efficacy of KRG on endocrine disrupting chemicals and OVX mouse.