• Journal of Korean Medicine for Obesity Research
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• v.5 no.1
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• pp.157-163
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• 2005

Obesity may induce an amenorrhea and ovulation disorder resulted from endocrine dysfunction, and so it is closely linked to infertility. Recently I've experienced a case that a woman complained of infertility with ovulation disorder, polycystic ovary and obesity has succeeded in pregnancy and delivery by the treatment of weight reduction during 2 months.

• Journal of Haehwa Medicine
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• v.9 no.1
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• pp.267-285
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• 2000

According to the literatural study on the causes of Infertility in women, the results were as follows. 1. The causes of Infertility in women were arranged scholarly thoery during to Jin-Yuan era (金 元 時代) from Huang-Di-Nei-Jing(黃帝內經), and literatures after Ming-Qing era(明 淸 時代) divided and added one's own thoery since they choose preceding thoery. 2. In the Modern Medicine, the causes of Infertility in women are divided the product obstruction of Oocyte, the union obstruction of sperm and oocyte by abnormality of vagina, cervix, corpus, fallopian tubes, pelvic, and peritoneum, Endocrine factor, Immunologic factor, and Emotion factor. 3. In the Oriental Medicine, the causes of Infertility in women are attached importance to functional side as 'asthenia-cool of uterus'(子宮虛寒), 'deficiency of vital energy and blood'(氣血虛), 'deficiency of yin'(陰虛), 'impairement of seven emotion'(七情傷), 'disease of extra mierdians'(寄經病), and so forth; while on the other in the Modern Medicine, the causes of Infertility in women are attached importance to organic side as abnormality of uterus and ovary. 4. In the successive literatures, 'asthenia-cool of uterus'(子宮虛寒) occupied most frequency in the causes of Infertility in women and in the next obesity(體肥), 'deficiency of vital energy and blood'(氣血虛), menstrual irregularity(月經不調), deficiency of yin'(陰虛), 'impairement of seven emotion'(七情傷), emaciation(體瘦), 'disease of extra mierdians'(寄經病), and so forth occupied much frequency. 5. In the bodily form, obesity(體肥) and emaciation(體瘦) occupied comparatively more frequency.

• Journal of Korean Medicine for Obesity Research
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• v.7 no.1
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• pp.31-38
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• 2007

Objective : Women's obesity brings prblems not only appearance but also health which men do not have. This study was conducted to investigate the different factors of obesity between men and women. Materials and Methods : We searched papers usin key words (women, gender, and obesity) on pubmed and obesity journal. Result : Women's obesity leads to amenorrhea, abnormal uterine bleeding, infertility, poly cystic ovarian syndrome, abortion, and luteal phase inadequacy. Obesity induces metabolic syndrome, type-2 diabetes, cardiovascular problems, hypertension, cancer, and psychophysiologic diseases. The difference in body morphology and in particular fat distribution between the sexes leads to gender-specific differences in prevalence of chronic diseases, and unique problems for each sex including infertility, problems during pregnancy, polycystic ovarian syndrome, and endometrial carcinoma in women, and prostate and testicular cancer in men. The influence of gender on obesity is had by genetic view, hormones, pregnancy, delivery, and menopause. Conclusion : Obese women have higher risk factors than men by the influence of gender.

• Clinical and Experimental Reproductive Medicine
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• v.44 no.1
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• pp.28-32
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• 2017

Objective: Growing evidence suggests that increased cardiovascular disease (CVD) risk is associated with female infertility caused by conditions such as polycystic ovarian disease, obesity, thyroid dysfunction, and endometriosis. The aim of this study was to evaluate whether any relationship exists between CVD and unexplained infertility. Methods: Sixty-five women with unexplained infertility and 65 fertile controls were enrolled in the study. CVD risk markers such as low-density lipoprotein (LDL), high-density lipoprotein (HDL), total cholesterol (TC), triglycerides (TG), insulin resistance (defined by the homeostasis model assessment ratio), and high-sensitivity C-reactive protein (hs-CRP) were assessed. Results: TG, TC, LDL, and hs-CRP levels were higher and HDL levels were lower in patients with unexplained infertility than in fertile controls (p<0.05 for all). Positive associations were found between unexplained infertility and TG, TC, LDL, and hs-CRP levels, and a negative correlation was found for HDL (p<0.05 for all). Multivariate logistic regression analysis showed that TG, HDL, and hs-CRP were independent variables associated with unexplained infertility. Conclusion: Our study showed that women with unexplained infertility had an atherogenic lipid profile and elevated hs-CRP levels, suggesting a higher risk of developing CVD in the future. Further studies with larger groups are needed to investigate the nature of this link.

• Clinical and Experimental Reproductive Medicine
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• v.40 no.3
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• pp.135-140
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• 2013

Objective: To evaluate correlations between serum anti-M${\ddot{u}}$llerian hormone (AMH) levels, phenotypes of polycystic ovary syndrome (PCOS), obesity, and metabolic parameters in patients with PCOS. Methods: A total of 175 patients with PCOS were diagnosed according to the Rotterdam Consensus were included. Exclusion criteria were age over 40, FSH>25 mIU/mL, and 17a-OHP>1.5 ng/mL. The Phenotypes of PCOS were divided into a severe form (oligo-anovulation, ANOV/hyperandrogenism/polycystic ovary morphology [PCOM]; n=59) and a mild form without HA (ANOV/PCOM, n=105). The serum AMH levels were classified into 3 groups (<5 vs. 5-10 vs. >10 ng/mL). Obesity was defined as body mass index (BMI) ${\geq}25kg/m^2$ (n=34). Results: The mean age was $25.9{\pm}5.7$ year and mean AMH level was $10.1{\pm}5.4$ ng/mL. The BMI ($kg/m^2$) was higher in group 1 ($24.2{\pm}6.3$) than in group 2 ($21.9{\pm}4.3$, p=0.046) or group 3 ($21.6{\pm}3.3$, p=0.019). There was no difference among the three groups in age, menstrual interval, antral follicle counts, androgens, or other metabolic parameters. The obesity group showed significantly lower AMH ($7.7{\pm}3.9$ ng/mL vs. $10.7{\pm}5.6$ ng/mL), p=0.004) and low-density lipoprotein levels ($93.1{\pm}21.2$ mg/dL vs. $107.5{\pm}39.3$ mg/dL, p=0.031), and showed higher total T ($0.74{\pm}0.59$ L vs. $0.47{\pm}0.36$ ng/mL, p=0.001), free T ($2.01{\pm}1.9$ vs. $1.04{\pm}0.8$ pg/mL, p=0.0001), and free androgen index ($6.2{\pm}7.9$ vs. $3.5{\pm}3.0$, p=0.003). After controlling for age factors and BMI, the serum AMH levles did not show any significant correlations with other hormonal or metabolic parmeters. Conclusion: For PCOS patients under the age 40, serum AMH is not negatively correlated with age. High serum AMH levels can not predict the phenotype of PCOS and metabolic disturbances in PCOS patients in the non-obese group. Further study might be needed to define the relation more clearly.

• Clinical and Experimental Reproductive Medicine
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• v.29 no.3
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• pp.209-214
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• 2002

Objective : To analyze the clinical characteristics of obese infertile women. Material and Method: Height, weight, body mass index, menstrual pattern, glucose, insulin, glucose/insulin ratio, dehydroepiandrosterone sulfate (DHEA-S), testosterone, free testosterone and plasminogen activator inhibitor (PAI-1) of 15 obese infertile women were tested. Results: Of 15 obese infertile women, the number of diabetes mellitus, hyperinsulinemia, and insulin resistance was 2 (13%), 2 (13%), 2 (13%), respectively. The incidence of increased DHEA-S, testosterone, and free testosterone was 7 (47%), 1 (7%), 6 (40%), respectively. Notably, all patients showed increased PAI-1. Conclusions: Obesity is associated with infertility as well as many kinds of health problems. Obesity is closely related to insulin resistance and it also causes hyperandrogenism. Increased PAI-1 is one of the important causes of thrombophilia. Consequently, in the workup of obese infertile patient, many aspects of health problems should be considered.

• Archives of Pharmacal Research
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• v.25 no.2
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• pp.178-183
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• 2002

A high molecular ar weight water-soluble chitosan (WSC) with an average molecular weight of 300 kD and a deacethylation level of over 90% was produced using a simple multi-step-membrane separation process. It is known that WSC prevents obesity induced by a high-fat diet. Consequently, this study investigated whether or not WSC improved the ovarian dysfunction caused by obesity in mice. The mice were fed a high density protein and lipid diet for weeks, followed by the administration of WSC at 480 mg/kg body weight per day for 4 days. Thereafter, the changes in body weight, ovulation rate, in vivo and in vitro fertilization and emboryonic development were measured . WSC markedly reduced the body weight of obese mice fed with a high-fat diet, but not in mice fed with a normal diet. WSC had siginificant effects on the ovulation rate, both the in vivo and in vitro fertilization rates and embryonic development. These results indicate an improvement in the ovarian and oviduct dysfunction caused by obesity, and suggest an adjustment in the internal secretions and metabolic functions.

• 대한생식의학회:학술대회논문집
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• 2006.06a
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• pp.157.2-157.2
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• 2006

• Clinical and Experimental Reproductive Medicine
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• v.38 no.2
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• pp.103-108
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• 2011

Objective: To investigate adverse pregnancy outcomes in non-obese women with polycystic ovary syndrome (PCOS) compared with obese-PCOS and control groups. Methods: Women with PCOS who underwent assisted reproductive technology (ART) from August, 2003 to December, 2007, were considered. A total of 336 women with PCOS were included in the study group and 1,003 infertile women who had tubal factor as an indication for ART were collected as controls. They were divided into four groups: a non-obese PCOS group, obese-PCOS group, non-obese tubal factor group, and obese tubal factor group, with obesity defined by a body mass index over 25 kg/$m^2$, and reviewed focusing on the basal characteristics, ART outcomes, and adverse pregnancy outcomes. Results: There was no difference among the groups' the clinical pregnancy rate or live birth rate. Regarding adverse pregnancy outcomes, the miscarriage rate, multiple pregnancy rate, and prevalence of preterm delivery and pregnancy induced hypertension were not different among the four groups. The incidence of small for gestational age infant was higher in the PCOS groups than the tubal factor groups ($p$ <0.02). On the other hand, the morbidity of gestational diabetes mellitus (GDM) was not high in the non-obese PCOS group but was in the obese groups. And in the obese PCOS group, the newborns were heavier than in the other groups ($p$ <0.02). Conclusion: Non-obese PCOS presents many differences compared with obese PCOS, not only in the IVF-parameters but also in the morbidity of adverse pregnancy outcomes, especially in GDM and fetal macrosomia.

• Clinical and Experimental Reproductive Medicine
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• v.28 no.2
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• pp.141-145
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• 2001

Objective: We inversigated Small Heterodimer Partner (SHP) gene mutation in Korean Polycystic Ovarian Syndrome (PCOS) patients. SHP protein regulates the activity of nuclear receptors which regulate the cellular development and differentiation. Recently, the mutation of SHP gene was found in the obesity and diabetes patients in Japanese group, and suggested that its mutation may involved in pathogenic mechanism of PCOS. Methods: This study was performed in 20 PCOS patients and 20 normal women. The DNAs were extracted from the peripheral bloods, and amplified at each exon (1 and 2) of SHP gene by PCR method. Subsequently, each PCR product was digested with the restriction enzyme indicated below for studying restriction fragment length polymorphism (RFLP). After enzyme digestion, the results of RFLP were compared PCOS patients with control women to find any sequence variation. Results: We examined 9 regions of exon 1 with Msp I, Pvu II, Dde I and 3 regions of exon 2 with Pst I, Dde I. There is no heterozygous or homozygous mutation in patients and control women at these restriction sites. Conclusion: The genetic analysis at our restriction sites in the SHP gene did not show any genetic variation in Korean PCOS patients. Our PCR-RFLP analysis was not covered the entire SHP gene (68 bp/1,006 bp), we need to further analysis of the entire SHP gene.