• Clinical and Experimental Reproductive Medicine
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• v.24 no.3
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• pp.355-359
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• 1997

Leiomyomas, which are the commonest pelvic tumors in women, are originated from myometrial cells. Although the exact initial pathophysiologic event of the leiomyoma is not known, recent evidences suggested that the effects of sex steroid hormones in the process of tumor growth are mediated by local production of growth factors including epidermal growth factor (EGF), insulin-like growth factor-I (IGF-I) and insulin-like growth factor-II (IGF-II). If we look at the effects of other cytokines, it was suggested that basic fibroblast growth factor (bFGF) may stimulate the proliferation of myometrial and leiomyomas cells. And it was reported that interferon-${\alpha}$ inhibit the action of bFGF. Therefore, we examined the effect of bFGF and interferon-${\alpha}$ on the proliferation of leiomyoma and myometrial cells. bFGF stimulated the myometrial and leiomyoma cells significantly at the concentration of 1ng/ml (p<0.05) and 5ng/ml (p<0.05). However, Interferon-${\alpha}$ inhibited the cell proliferation of myometrial and leiomyoma cells significantly at the concentration of 100U/ml (p<0.05) and 1000U/ml (p<0.05). And the stimulated effects of bFGF with the various concentration on the myometrial and leiomyoma cells ware inhibited by interferon-${\alpha}$ with 100U/ml. Therefore, we concluded that bFGF may stimulate the myometrial and leiomyoma cell proliferation and interferon-${\alpha}$ may inhibit the myometrial and leiomyoma cell proliferation through blocking the effect of basic fibroblast growth factor.

• Development and Reproduction
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• v.8 no.2
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• pp.99-111
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• 2004

The present study aimed to investigate whether the expression of ADAM-8, 9, 10, 12, 15, 17 and ADAMTS-1 genes is controlled by ovarian steroid hormones. Ovariectomized mice were injected with 17 ${\beta}$-estradiol ($E_2$), progesterone ($P_4$, or $E_2+P_4$. Uterine tissues were processed for RT-PCR and immunoblotting. The results of RT-PCR showed that administration of $E_2$ increases the level of ADAM-8, 12 and ADAM17 expression compared to $P_4$ or control group. In contrast, administration of $P_4$ markedly stimulated the expression of ADAM-9, 10, 15 and ADAMTS-1, whereas $E_2$ did not. Immunoblotting analysis using anti-mouse ADAM polyclonal antibodies demonstrated that $E_2$ alone or $E_2+P_4$ treatment results in the strong expression of ADAM-8, 12 and ADAM17 proteins but $P_4$ alone or control group gave weak expression. In contrast, $P_4$ alone or $E_2$ plus $P_4$ treatment increased the expression level of ADAM-9, 10, 15 and DAMTS-1 proteins. $E_2$ alone or control group did not increase the expression. These results indicate that expression of ADAM-8, 12 and ADAM17 genes is upregulated by $E_2$ and that of ADAM-9, 10, 15 and ADAMTS-1 gene is upregulated by $P_4$.

• Development and Reproduction
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• v.10 no.4
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• pp.247-254
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• 2006

It is well publicized that the existence of various endocrine disrupting chemicals threatens normal sexual development of many sedentary marine fishes in the coastal areas. However, a suitable marine fish species for efficient monitoring of this threatening has yet to be identified. One of the difficulties in estimating the effect of endocrine disruption in marine fish is the absence of clear distinction between testicular and ovarian structures at the early stages of sex differentiation. In search of a potential test species, we have investigated the microscopic structures of sexually undifferentiated and differentiated gonads and the susceptibility of gonadal differentiation to exogenous sex steroids during the sex differentiation period in a sedentary marine rockfish, Sebastes schlegeli. Male gonads in this species contained dark pigmentation that made them distinct from female gonads. Treatment either with $estradiol-17\;{\beta}(E_2)$ or $17\;{\alpha}-methyltestosterone$ (MT) significantly altered the sex ratios with the complete sex changes or the occurrence of ovotestis that was easily identified by the mixed structure of dimorphic gonads (coexistence of ovarian cavity/primary oocytes and dark pigmentation/seminiferous tubules). Results in this study suggest that S. schlegeli can be developed as a monitoring/test fish species for endocrine disruption in marine fish in the coastal areas.

• Development and Reproduction
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• v.22 no.4
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• pp.379-391
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• 2018

Through the development of organic synthetic skill, chemicals that mimic signaling mediators such as steroid hormones have been exposed to the environment. Recently, it has become apparent that this circumstance should be further studied in the field of physiology. Estrogenic action of chronic low-dose nonylphenol (NP) and di-(2-ethylhexyl) phthalate (DEHP) in mouse uterus was assessed in this study. Ten to twelve-week-old female mice (CD-1) were fed drinking water containing NP (50 or $500{\mu}g/L$) or DEHP (133 or $1,330{\mu}g/L$) for 10 weeks. Uterine diameter, the thickness of myometrium and endometrium, and the height of luminal epithelial cells were measured and the number of glands were counted. The expression levels of the known $17{\beta}$-estradiol ($E_2$)-regulated genes were evaluated with real-time RT-PCR methodology. The ration of uterine weight to body weight increased in $133{\mu}g/L$ DEHP. Endometrial and myometrial thickness increased in 133 and $1,330{\mu}g/L$ DEHP treated groups, and in 50, $500{\mu}g/L$ NP and $133{\mu}g/L$ DEHP, respectively. The height of luminal epithelial cell decreased in NP groups. The numbers of luminal epithelial gland were decreased in NP groups but increased in $50{\mu}g/L$ DEHP group. The histological characters of glands were not different between groups. The mRNA expression profiles of the known $17{\beta}$-estradiol ($E_2$) downstream genes, Esr1, Esr2, Pgr, Lox, and Muc1, were also different between NP and DEHP groups. The expression levels dramatically increased in some genes by the NP or DEHP. Based on these results, it is suggested that the chronic low-dose NP or DEHP works as estrogen-like messengers in uterus with their own specific gene expression-regulation patterns.

• Journal of Life Science
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• v.33 no.9
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• pp.693-702
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• 2023

The present study examined the rate of cell growth and differentiation potential into adipocytes in A549 lung adenocarcinoma cells exposed to each adipogenic medium containing glucose metabolism hormones, such as thyroxine (T4) thyroid hormone and glucocorticoid (GC) adrenal steroid hormone, as well as pioglitazone (PGZ), a PPARγ agonist. Following each adipogenic treatment for 2 weeks, the rate of cell growth was significantly (p<0.05) inhibited, and the level of telomerase activity was significantly (p<0.05) decreased in the PGZ-based adipogenic medium containing both T4 and GC hormone compared with those containing each T4 or GC hormone. Moreover, the adiposome-like vesicles were highly reacted with Oil-Red O staining solution, and the levels of transcripts expressed in the differentiating adipocytes for adipogenesis, including adinopectin, leptin, and resistin, were significantly (p<0.05) increased in the PGZ-based adipogenic medium containing both T4 and GC hormone compared with those of the adipogenic medium containing each T4 or GC hormone, implying that adipocytic differentiation has fully occurred in the A549 cancer cells. Based on present observations, the PGZ-based adipogenic medium containing both T4 and GC efficiently induces inhibition of cell growth and cellular differentiation into adipocytes in A549 cancer cells rather than in the adipogenic medium containing only T4 or GC hormone. Adipogenic treatment could provide potential probability in cancer chemotherapy.

• Korean Journal of Exercise Nutrition
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• v.16 no.2
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• pp.65-71
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• 2012

Oxygen is the final acceptor of electron transport from fat and carbohydrate oxidation, which is the rate-limiting factor for cellular ATP production. Under altitude hypoxia condition, energy reliance on anaerobic glycolysis increases to compensate for the shortfall caused by reduced fatty acid oxidation [1]. Therefore, training at altitude is expected to strongly influence the human metabolic system, and has the potential to be designed as a non-pharmacological or recreational intervention regimen for correcting diabetes or related metabolic problems. However, most people cannot accommodate high altitude exposure above 4500 M due to acute mountain sickness (AMS) and insulin resistance corresponding to a increased levels of the stress hormones cortisol and catecholamine [2]. Thus, less stringent conditions were evaluated to determine whether glucose tolerance and insulin sensitivity could be improved by moderate altitude exposure (below 4000 M). In 2003, we and another group in Austria reported that short-term moderate altitude exposure plus endurance-related physical activity significantly improves glucose tolerance (not fasting glucose) in humans [3,4], which is associated with the improvement in the whole-body insulin sensitivity [5]. With daily hiking at an altitude of approximately 4000 M, glucose tolerance can still be improved but fasting glucose was slightly elevated. Individuals vary widely in their response to altitude challenge. In particular, the improvement in glucose tolerance and insulin sensitivity by prolonged altitude hiking activity is not apparent in those individuals with low baseline DHEA-S concentration [6]. In addition, hematopoietic adaptation against altitude hypoxia can also be impaired in individuals with low DHEA-S. In short-lived mammals like rodents, the DHEA-S level is barely detectable since their adrenal cortex does not appear to produce this steroid [7]. In this model, exercise training recovery under prolonged hypoxia exposure (14-15% oxygen, 8 h per day for 6 weeks) can still improve insulin sensitivity, secondary to an effective suppression of adiposity [8]. Genetically obese rats exhibit hyperinsulinemia (sign of insulin resistance) with up-regulated baseline levels of AMP-activated protein kinase and AS160 phosphorylation in skeletal muscle compared to lean rats. After prolonged hypoxia training, this abnormality can be reversed concomitant with an approximately 50% increase in GLUT4 protein expression. Additionally, prolonged moderate hypoxia training results in decreased diffusion distance of muscle fiber (reduced cross-sectional area) without affecting muscle weight. In humans, moderate hypoxia increases postprandial blood distribution towards skeletal muscle during a training recovery. This physiological response plays a role in the redistribution of fuel storage among important energy storage sites and may explain its potent effect on changing body composition. Conclusion: Prolonged moderate altitude hypoxia (rangingfrom 1700 to 2400 M), but not acute high attitude hypoxia (above 4000 M), can effectively improve insulin sensitivity and glucose tolerance for humans and antagonizes the obese phenotype in animals with a genetic defect. In humans, the magnitude of the improvementvaries widely and correlates with baseline plasma DHEA-S levels. Compared to training at sea-level, training at altitude effectively decreases fat mass in parallel with increased muscle mass. This change may be associated with increased perfusion of insulin and fuel towards skeletal muscle that favors muscle competing postprandial fuel in circulation against adipose tissues.

• Journal of Life Science
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• v.19 no.5
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• pp.593-597
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• 2009

The uterus plays a critical role in pregnancy and steroid hormones, and both estrogen (E2) and progesterone (P4) especially play important roles in the cross-talk between embryos and uterus to support the pregnancy. E2 stimulates uterine growth during early pregnancy to prepare for implantation of embryos. This cross-talk during the implantation period involves hormones (E2 and P4) and growth factors, including insulin-like growth factor-I (IGF-I). In the uterus of a pregnant pig, the action of E2 is mediated by estrogen receptor-${\beta}$ (ER-${\beta}$). The expression of ER-a was much higher in early pregnancy than in mid- and late- pregnancy, suggesting E2 secretion from embryos enhances transcription of ER-a during early pregnancy. In order to prove whether IGF-I is an E2 target gene, quantitative real-time PCR was performed on ovariectomized murine uterus with E2 and/or P4 treatment(s). Increased IGF-I mRNA expression was observed with E2 treatment, however, it was not significantly induced by P4 treatment, which clearly demonstrates that, in mice, E2 depends on the activation of uterine IGF-I gene expression. The expression of IGF-I in the uterus of pigs was much higher in early pregnancy than in mid- and late- pregnancy and these data exhibited the same expression pattern with the ER-${\beta}$ gene expression in the uterus. It suggests that a positive co-relationship between IGF-I and ER-${\beta}$ expression exists in the uterus, and that both gene expressions of IGF-I and ER-${\beta}$ are regulated by E2. It further suggests that uterine the IGF-I gene expression might be initiated by E2 secreted from embryos to increase ER-${\beta}$ gene expression, and that this increased ER-${\beta}$ further stimulates the expression of IGF-I in the uterus during early pregnancy.

• Development and Reproduction
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• v.6 no.2
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• pp.105-110
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• 2002

Numerous hormones are involved in the regulation of reproduction. Among them, estrogen and progesterone are the most important ovarian steroid hormones regulating female fertility. On the other hand, diverse stressors impede female receptivity and fertility. Since norepinephrine(NE) and epinephrine(E) are released from the adrenal during stress, it might play a role in stress-induced disruptions of fEmale reproductive parameters. The present study was performed to analyze the changes in adrenal catecholaminergic activities in cycling rats. The tissue content and secretion level of catecholamines were determined by high performance liquid chromatography coupled with electrochemical detector(HPLC-ECD). Adrenomedullary content of norepinephrine(NE) was increased on proestrus stage (59.47 $\pm$ 6.86 ug/gland), peaked on diestrus I stage(65.22 $\pm$ 5.99 ug/gland), and was nadir on diestrus II stage(41.63 $\pm$ 1.33 ug/gland). The highest E content was observed on proestrus stage(361.86 $\pm$ 15.58 ug/gland) while the lowest level was on diestrus II stage(285.58 $\pm$ 12.25 ug/gland). In addition to these observations, a significant reduction of the NE : E ratio was observed (1 : 4.81 on diestrus I vs 1 : 6.13～7.02 on other stages). In vitro secretion of adrenal NE and E was increased on proestrus stage, peaked on estrus stage, and decreased on diestrus II stage. Interestingly, the NE : E ratio in conditioned media was significantly increased on estrus stage (1 : 3.32 vs 1 : 2.34～2.65 on other stages. The biosynthesis of NE and E is mediated by tyrosine hydroxylase(TH) and phenylethanolamine-N-methyltransferase(PNMT) which acts conversion of tyrosine into DOPA and NE into E, respectively. These finding demonstrated that sex steroids, during setrous cycle, seem to be able to modify the adrenal catecholamines biosynthesis and secretion with stage-specific manner by modulation of the enzyme activities.

• Korean Journal of Fisheries and Aquatic Sciences
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• v.30 no.2
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• pp.203-210
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• 1997

The aim of this study was to determine the effect of steroids and human chorionic gonadotropin (HCG) on in vitro maturation and ovulation of oocyte in Pseudobagrus fulvidraco. Oocytes were incubated in the media Leibovitz L15 supplemented with the various concentration of $17\alpha,\;20\beta-dihydroxy-4-pregnen-3-one(17\alpha20{\beta}OHP),\;17\alpha-hydroxyprogesterone(17{\alpha}OHP),\;progesterone(P_4),\;estradiol-17\beta(E_2)and\;HCG$. After 60 hours incubation, the maturation ability of oocyte was assessed by the appearance of germinal vesicle breakdown (GVBD). GVBD was significantly enhanced by the addition of $17\alpha20{\beta}OHP,\;17{\alpha}OHP,\;P_4\;and\;HCD(P<0.05)$. The highest CVBD was observed when $17\alpha20{\beta}OHP$ and HCG were supplemented to media. When oocytes were cultured for 16 hours in media containing $10\~1,000\;ng/ml\;17\alpha20{\beta}OHP,\;17{\alpha}OHP\;and\;P_4$, the rate of GVBD in oocytes cultured in the medium supplemented with 100 ng/ml $17\alpha20{\beta}OHP(65\%)$ was significantly higher than that with $17{\alpha}OHP\;(40\%)\;and\;P_4(35\%)$. The efforts of $17\alpha20{\beta}OHP$ and HCG on GVBD were assessed by various concentration of these hormones. When oocytes were cultured for 60 hours in various media containing $1\~1,000\;ng/ml\;17{\alpha}20{\beta}OHP\;or\;5\~1,000\;IU/ml$ HCG, the GVBD of oocytes was significantly increased in the medium with $10\~100\;ng/ml\;17\alpha20{\beta}OHP$ and 500 IU/ml HCT. When oocytes were cultured in the various media supplemented with $1\~1,000\;ng/ml\;17\alpha20{\beta}OHP\;or\;5\~1,000\;IU/ml$ HCG for 60 hours, the media with $1\~100\;ng/ml\;17\alpha20{\beta}OHP\;or\;50\~1,000IU/ml$ HCG significantly increased in the rate of ovulation. However supplementation with $1,000\;ng/ml\;17\alpha20{\beta}OHP$or 5 IU/ml HCG did not improve the rate of ovulation compared to controls. This results indicate that supplementation of steroid and HCG except $E_2$ can improve the in vitro maturation and ovulation of oocyte in P. fulvidrac; HCG and $17\alpha20{\beta}OHP$ may be more effective than other steroids on oocyte maturation and ovulation in P. fulvidraco.

• Korean Journal of Agricultural Science
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• v.8 no.1
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• pp.64-71
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• 1981

The present study was carried out to study the serum concentration of peptide and steroid hormones in puerperal sow. Eight crossbred sows were used for collection of blood samples from day 20 prepartum to day 20 postpartum. FSH, LH, prolactin, estradiol-$17{\beta}$, progesterone and cortisol were assayed by radioimmunoassay methods. The mean serum FSH did not vary during the puerperal period and ranged from $8.1{\pm}1.8mIU/ml$ to $9.0{\pm}2.3mIU/ml$. LH concentrations increased from $2.6{\pm}0.3mIU/ml$ at day 20 prepartum to $3.9{\pm}1.1mIU/ml$ at the time of parturition, reached $3.2{\pm}0.9mIU/ml$ by day+2 and remained quite constant therafter. Prolactin reached a peak mean level of $68.5{\pm}9.5ng/ml$ at day 0. Estradiol-$17{\beta}$ increased from $205.0{\pm}29.5pg/ml$ at day 6 prepartum to $425.0{\pm}35.0pg/ml$ at the time of parturition. Progesterone remained fairly constant ($18.4{\pm}1.6$ to $20.2{\pm}2.1ng/ml$) from 20 to 6 days before parturition, began to decline on day-2, reached $0.9{\pm}0.3ng/ml$ by day+2 and remained quite constant thereafter. Cortisol reached a peak level of $86.5{\pm}10.5ng/ml$ at the day 0.