• 대한생식의학회:학술대회논문집
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• 2007.06a
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• pp.95-102
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• 2007

• 대한생식의학회:학술대회논문집
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• 1997.06a
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• pp.14-15
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• 1997

• 대한약리학회:학술대회논문집
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• 2006.10a
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• pp.76-76
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• 2006

• Clinical and Experimental Reproductive Medicine
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• v.23 no.3
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• pp.269-275
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• 1996

Biosynthesis and secretion of anterior pituitary hormones are under the control of specific hypothalamic stimulatory and inhibitory factors. Among them, Growth Hormone Releasing Hormone (GHRH) is the major stimulator of pituitary somatotrophs activating GH gene expression and secretion. Human GHRH is a polypeptide of 44 amino acids initially isolated from pancreatic tumors, and the gene for the hypothalamic form of GHRH is organized into 5 exons spanning over 10 kilobases (kb) on genomic DNA and encodes a messenger RNA of 700-750 nucleotides. Several neuropeptides classically associated with the hypothalamus have been found in the extrahypothalamic regions, suggesting the existence of novel sources, targets and functions. GHRH-like immunoreactivity has been found in several peripheral sites, including placenta, testis, and ovary, indicating that GHRH may also have regulatory roles in peripheral reproductive organs. Furthermore, higher molecular weight forms of the GHRH transcripts were identified from these organs (1.75 kb in testis; 1.75 and >3 kb in ovary). These tissue-specific expression of GHRH gene suggest the existence of unique regulatory mechanism of GHRH expression and function in these organs. In fact, placenta-specific and testis-specific promoters for GHRH transcripts which are located in about 10 kb upstream region of hypothalamic promoter were reported. The use of unique promoters in extrahypothalamic sites could be refered in a different control of GHRH gene and different functions of the translated products in these tissues. Somatotrophs and lactotrophs have been thought to be derived from a common bipotential progenitor, the somatolactotrophs, which give origins to either phenotypes. Although the precise mechanism responsible for the lactotroph differentiation in the anterior pituitary gland has not been yet clalified, there are several candidators for the generation of lactotrophs. In human, the presence of GHRH peptides with different size from authentic hypothalamic form in the normal anterior pituitary and several types of adenoma were demonstrated. Recently our group found the existence of immunoreactive GHRH and its transcript from the normal rat anterior pituitary (gonadotroph> somatotroph> lactotroph), and the GHRH treatment evoked the increased proliferation rate of anterior pituitary cells in vitro. The transgenic mouse models clearly shown that GHRH or NGF overexpression by anterior pituitary cells induced development of pituitary hyperplasia and adenomas particularly GH-oma and prolactinoma. Taken together, we hypothesize that the pituitary GHRH could serve not only as a modulator of hormone secretion but as a paracrine or autocrine regulator of anterior pituitary cell proliferation and differentiation. Interestingly enough, the expression of Pit-1 homeobox gene (the POU class transcription factor) was confined to somatotrophs, lactotrophs and somatolactotrophs in which GHRH receptors are expressed commonly. Concerning the mechanism of somatolactotroph and lactotroph differentiation in the anterior pituitary, we have focused following two possibilities; (1) changes in the relative levels or interactions of both hypothalamic and intrapituitary factors such as dopamine, VIP, somatostatin, NGF and GHRH; (2) alterations of GHRH-GHRH receptor signaling and Pit-1 activity may be the cause of lactotroph differentiation or pituitary hyperplasia and adenoma formation. Extensive further studies will be necessary to solve these complicated questions.

• The Korean Journal of Zoology
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• v.39 no.4
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• pp.337-351
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• 1996

Melatonin Is a multifunctional hormone secreted from the pineal gland in the middle of cerebrum and cerebellum. Its synthesis and release reflect photopedod;Photopedod is a yearly predictable ambient factor that most animals utilize as an environmental cue for maximum survival. Hamsters maintaln reproductive activity in summer during which day length exceeds night time. Upon the advent of autumnal equinox they undergo gonadal regression. The photoperiodic effects are prevented by removal of the pineal gland and restored by the timed repiacument of melatonin. The results suggest that melatonin constitutes part of control mechanism whereby environmental information is transduced to neuroendocrine signal responsIble for the functional integrity of the reproductive system. From the studies for the action site of melatonin following the treatment of photopedod or melatonin in the lesion of a spedflc portion of hypothalamus, suprachiasmatic nuclei and pars tuberalis are shown to be a consensus site for melatonIn. The action of melatonin. In the regulation of reproduction is largely unknown. It is mainly due to the lack of acute effect of melatonin on gonadotropin secretion. However, reduction of the gonadotropln release and augmentation of the hypothalamic gonadotropin-releasing hormone (GnRH) content by long-term treatment of melatonln Indicate that constant presence of melatonln may partidpate in the regulation of sexual activity via the GnRH neuronal system. The action mechanism by which melatonin exerts Its effect on GnRH neuron needs to be eluddated. The inability of opiold analogues to affect the reproductive hormones in sexually regressed animals by inhibftory photopedod and melatonin suggests that the opioldergic neuron may be a prime intervening mediator. Recent cloning of melatonin receptor will contribute to investigate its anatomical Identification and the action mechanism of melatonin on target tissues at the molecular level.

• Korean Journal of Environmental Biology
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• v.20 no.3
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• pp.224-231
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• 2002

Photoperiod (length of light per day) is a major factor in regulating reproductive function in golden hamsters. The information of photoperiod is transmitted to the reproductive endocrine system by melatonin. Thus the effects of melatonin aye investigated in male golden hamsters exposed to photoperiods. Paired testicular weights were markedly reduced in the animals housed in short photoperiod $(SP,\le{12\;hours\;day^{-1})$ and injected with melatonin in the evening, but not in long photoperiod $(LP,\le{12.5}\;hours\;day^{-1})$ and injected with melatonin in the morning. The histological examination of regressed testes showed reduction of tubular lumen diameter including the numbers of cells and Leydig cell number. The mean values of both follicle stimulating hormone (FSH) and luteinizing hormone (LH) were also lowered in the sexually inactive animals than in the sexually active animals. Melatonin receptor was identified by reverse-transcription polymerase chain reaction (RT-PCR) and its expression was examined in various tissues to scrutinize the action site of melatonin. It turned out 309 nucleotides and was definitely expressed in hypothalamus and pituitary including spleen, retina, and epididymis. And gonadotropin releasing hormone (GnRH) gene, which is a key element in regulating reproduction, was identified by RT-PCR but the expression of GnRH was not modified by the treatment of melatonin. Taken together, photoperiod via melatonin indirectly affects reproductive endocrine system, possibly through the release of GnRH, not the synthesis of GnRH.

• Clinical and Experimental Reproductive Medicine
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• v.36 no.3
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• pp.225-230
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• 2009

Over the last several decades, the incidence of malignant melanoma has been increasing rapidly. The annual incidence rates have increased approximately 3~7% in Caucasian population. The rate of increase is highest in perimenopausal period in women. The relationship between risk of melanoma and female hormone is still unclear. The safety of hormone therapy for the melanoma patients is not known. We experienced a case of melanoma in whom underwent hormone therapy for 10 years. We report this case with a brief review of literature.

• Clinical and Experimental Reproductive Medicine
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• v.45 no.4
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• pp.183-188
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• 2018

Objective: The purpose of this retrospective study was to evaluate the appropriateness of various follicle-stimulating hormone (FSH) starting doses in expected normal responders based on the nomogram developed by La Marca et al. Methods: A total of 117 first in vitro fertilization cycles performed from 2011 to 2017 were selected. All women were expected normal responders and used a recombinant FSH and flexible gonadotropin-releasing hormone antagonist protocol. The FSH starting dose was empirically determined (150, 225, or 300 IU). The FSH starting dose indicated by La Marca's nomogram was determined using female age and serum $anti-M{\ddot{u}}llerian$ hormone or basal FSH levels. If the administered dose was exactly the same as the proposed dose, the cycle was assigned to the concordant group (34 cycles). If not, it was assigned to the discordant group (83 cycles). Optimal ovarian response was defined as a total of 8-14 oocytes, hypo-response as < 8 oocytes, and hyper-response as > 14 oocytes. Results: Between the concordant and discordant group, ovarian response (optimal, 32.4% vs. 27.7%; hypo-response, 55.9% vs. 54.2%; and hyper-response, 11.8% vs. 18.1%) and the number of total or mature oocytes were similar. Ovarian hyperstimulation syndrome was rare in both groups (0% vs. 1.2%). The implantation rate, clinical pregnancy rate, miscarriage rate, and live birth rate were all similar. Conclusion: The use of the proposed FSH starting dose determined using La Marca's nomogram did not enhance the optimal ovarian response rate or pregnancy rate in expected normal responders. Individualization of the FSH starting dose by La Marca's nomogram appears to have no distinct advantages over empiric choice of the dose in expected normal responders.

• Clinical and Experimental Reproductive Medicine
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• v.51 no.1
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• pp.48-56
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• 2024

Objective: This study investigated the relationship of anthropometric and metabolic risk factors with seminal and sex steroidal hormone parameters in a screened population of healthy males. Methods: The participants were healthy young men without chronic or congenital diseases. The body composition parameters that we investigated were measured weight, height, and waist circumference (WC), as well as bioelectrical impedance analysis. Semen samples were analyzed for semen volume, sperm concentration, sperm motility and morphology, seminal pH, and liquefaction time. Biochemistry analysis, including glucose and lipid metabolism parameters, was conducted on fasting blood samples. Testicular volume was calculated separately for each testis using ultrasonography. Results: Body mass index exhibited an inverse association with total sperm count. WC showed negative correlations with numerous seminal parameters, including sperm concentration, total sperm count, sperm morphology, and follicle-stimulating hormone levels. The basal metabolic rate was associated with seminal pH, liquefaction time, and sperm motility. WC, fat mass percentage, and triglyceride levels exhibited negative correlations with sex hormone binding globulin. The measures of glucose metabolism were associated with a greater number of seminal parameters than the measures of cholesterol metabolism. C-reactive protein levels were inversely associated with sperm concentration and total sperm count. Conclusion: Anthropometric and metabolic risk factors were found to predict semen quality and alterations in sex steroidal hormone levels.

• Animal Bioscience
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• v.37 no.1
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• pp.50-60
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• 2024

Objective: Testicular fat deposition has been reported to affect animal reproduction. However, the underlying mechanism remains poorly understood. The present study explored whether sperm meiosis and testosterone synthesis contribute to mouse testicular fat deposition-induced reproductive performance. Methods: High fat diet (HFD)-induced obesity CD1 mice (DIO) were used as a testicular fat deposition model. The serum hormone test was performed by agent kit. The quality of sperm was assessed using a Sperm Class Analyzer. Testicular tissue morphology was analyzed by histochemical methods. The expression of spermatocyte marker molecules was monitored by an immuno-fluorescence microscope during meiosis. Analysis of the synthesis of testosterone was performed by real-time polymerase chain reaction and reagent kit. Results: It was found that there was a significant increase in body weight among DIO mice, however, the food intake showed no difference compared to control mice fed a normal diet (CTR). The number of offspring in DIO mice decreased, but there was no significant difference from the CTR group. The levels of follicle-stimulating hormone were lower in DIO mice and their luteinizing hormone levels were similar. The results showed a remarkable decrease in sperm density and motility among DIO mice. We also found that fat accumulation affected the meiosis process, mainly reflected in the cross-exchange of homologous chromosomes. In addition, overweight increased fat deposition in the testis and reduced the expression of testosterone synthesis-related enzymes, thereby affecting the synthesis and secretion of testosterone by testicular Leydig cells. Conclusion: Fat accumulation in the testes causes testicular cell dysfunction, which affects testosterone hormone synthesis and ultimately affects sperm formation.