Ji Won Yoon

Dr. Ji Won Yoon


Research Focus & Metrics

Academic Career Length

11Years (2016-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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30 June 2019 in Journal of Obesity & Metabolic Syndrome
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Journal Article
Open access
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GCGoh Eun Chung
Goh Eun Chung
MKMin Joo Kim
Min Joo Kim
JYJeong Yoon Yim
Jeong Yoon Yim
JKJoo Sung Kim
Joo Sung Kim
JYJi Won Yoon
Ji Won Yoon
Goh Eun Chung, Min Joo Kim, Jeong Yoon Yim, Joo Sung Kim, Ji Won Yoon. JOMES 2019;28:129-38. https://doi.org/10.7570/jomes.2019.28.2.129

29 March 2021 in Frontiers in Medicine
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Journal Article
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GCGoh Eun Chung
Goh Eun Chung
HPHyo Eun Park
Hyo Eun Park
HLHeesun Lee
Heesun Lee
MKMin Joo Kim
Min Joo Kim
SCSu-Yeon Choi
Su-Yeon Choi
JYJi Won Yoon
Ji Won Yoon
Background: An association between sarcopenic obesity and cardiovascular disease has been suggested. We investigated the relationship between sarcopenia and coronary atherosclerosis, taking into account the presence or absence of obesity in a health check-up population.Methods: Data were reviewed for subjects who underwent bioelectrical impedance analysis (BIA) and coronary calcium scoring (CAC) computed tomography between January 2017 and December 2018. Appendicular skeletal muscle mass (ASM) was assessed using BIA. Sarcopenia was defined as reduction of muscle mass and calculated as ASM% (ASM/body weight) more than two standard deviations below the sex-specific mean for healthy young adults. CAC scores were dichotomized as low (<100) or high (≥100).Results: Among 1,282 subjects (mean age, 58.1 years; 75.5% male), the prevalence of high CAC was 21%. When the study population was divided into four groups according to their obesity and sarcopenia status, the prevalence of high CAC in the sarcopenic-obesity (SO) group was significantly higher than in the other groups (40.7%, P < 0.001). After adjusting for age, sex, hypertension, diabetes, dyslipidemia, and creatinine, subjects with SO exhibited a significantly higher odds of a high CAC score, compared with the non-sarcopenic, non-obese group (odds ratio, 1.92; 95% confidence interval, 1.16–3.18, P = 0.011).Conclusion: SO was significantly associated with CAC, independent of known risk factors for coronary artery disease. These findings suggest that sarcopenia and obesity may potentiate each other to increase atherosclerotic burden in coronary arteries, which may eventually lead to adverse cardiovascular events.

1 January 2020 in Human Fertility
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Journal Article
Closed access
JKJin Ju Kim
Jin Ju Kim
JYJi Won Yoon
Ji Won Yoon
MKMin Joo Kim
Min Joo Kim
SKSun Mie Kim
Sun Mie Kim
KHKyu Ri Hwang
Kyu Ri Hwang
YCYoung Min Choi
Young Min Choi
This study was performed to compare the prevalence of autoimmune thyroid disease (AITD) assessed by thyroid peroxidase antibody (anti-TPO Ab) and thyroid ultrasonography (USG) in Korean women with polycystic ovary syndrome (PCOS) (n = 210) and age-matched controls (n =343). We also compared the clinical features of women with PCOS according to the presence of AITD. Patients and controls were enrolled from a population who visited a screening centre for a general health check-up. There was no difference in the frequency of anti-TPO Ab positivity between the women with PCOS and the controls (4.8% (5/104) in patients and 7.6% (18/238) in controls). The frequency of heterogeneous or hypoechoic parenchyma on USG also did not differ between the patients and controls (9.3% (11/118) in patients and 12.3% (40/325) in controls). Within the PCOS group, the subjects with AITD (who had either Ab positivity or sonographic findings compatible with thyroiditis) showed significantly higher body mass indexes, waist circumferences and homeostasis model assessment for insulin resistance levels than the patients without AITD. In conclusion, AITD was not more prevalent in women with PCOS than in controls. However, among women with PCOS, subjects with AITD showed significantly higher adiposity and insulin resistance index than those without AITD.

12 October 2022 in Journal of Cachexia, Sarcopenia and Muscle
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Journal Article
Open access
JSJi Yeon Seo
Ji Yeon Seo
ECEun Ju Cho
Eun Ju Cho
MKMin Joo Kim
Min Joo Kim
MKMin‐Sun Kwak
Min‐Sun Kwak
JYJong In Yang
Jong In Yang
GCGoh Eun Chung
Goh Eun Chung
Background: Metabolic (dysfunction)‐associated fatty liver disease (MAFLD) emphasizes the metabolic dysfunction in nonalcoholic fatty liver disease (NAFLD). Although the relationship between low muscle mass and NAFLD has been suggested, the effect of MAFLD on low muscle mass is yet to be investigated. In this study, we examined the relationship between MAFLD and low muscle mass in an asymptomatic Korean population.Methods: Examinees who underwent FibroScan® and bioelectrical impedance analyses on the same day during the period of June 2017 to December 2019 were included. Hepatic steatosis was diagnosed using controlled attenuation parameter (CAP) with two cut‐off values of 248 and 294 dB/m. Low muscle mass was defined based on appendicular skeletal muscle mass/body weight (wt) or body mass index (BMI) ratios of two standard deviations below the sex‐specific mean for healthy young adults. Subjects were divided into four subgroups: diabetic MAFLD (presence of diabetes mellitus [DM]), metabolic dysfunction (MD) MAFLD (≥2 metabolic abnormalities without DM), overweight MAFLD (overweight/obese without DM and <2 metabolic abnormalities) and no MAFLD.Results: Among all of the 6414 subjects (mean 53.9 years of age; 85.4% male), the prevalence of MAFLD was 49.9% and 22.7% for CAP cut‐off values of 248 and 294 dB/m, respectively. In the multivariate analysis, MAFLD was associated with an increased risk of both low muscle mass_wt (odds ratio [OR] 1.80, 95% confidence interval [CI] 1.38–2.35, P < 0.001) and low muscle mass_BMI (OR 1.31, 95% CI 1.01–1.70, P = 0.042). The risk of low muscle mass_wt and low muscle mass_BMI increased the most in the diabetic MAFLD subgroup compared with the no‐MAFLD group (OR 2.11, 95% CI 1.51–2.96, P < 0.001 and OR 1.51, 95% CI 1.08–2.13, P = 0.017). There was an increased risk of low muscle mass_wt in the MD MAFLD subgroup (OR 1.73, 95% CI 1.31–2.28, P < 0.001). Comparable results were observed when the CAP cut‐off value of 294 dB/m was applied.Conclusions: The presence of MAFLD is significantly associated with increased risk of low muscle mass with varying risks according to the MAFLD subgroups. Clinicians should be aware of the differentiated risk of low muscle mass across the subgroups of MAFLD.

28 June 2016 in Cardiovascular Diabetology
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LKLee Kyung Kim
Lee Kyung Kim
JYJi Won Yoon
Ji Won Yoon
DLDong-Hwa Lee
Dong-Hwa Lee
Kyoung Min KimKyoung Min Kim
Kyoung Min Kim
SCSung Hee Choi
Sung Hee Choi
SLSoo Lim
Soo Lim
It is not clear how severe metabolic syndrome (MS) affects the development of coronary atherosclerosis. This was an observational, retrospective cohort study with Koreans who received health check-ups voluntarily. A total of 2426 subjects had baseline and follow-up coronary artery calcium score (CACS) data. Among them, 1079 had coronary computed tomography angiography (CCTA) data. We compared baseline CACS and any progression in subjects with and without MS. A more detailed analysis was conducted for coronary artery disease (CAD), which was defined by coronary artery stenosis (≥50 %), multivessel involvement, and coronary plaques in those patients with CCTA data. At baseline, subjects with MS (34.0 %, n = 825) had higher CACS and more significant coronary artery stenosis, multivessel involvement, and atheromatous plaques than those without MS (P < 0.05 for all). In the follow-up (median 1197 days), subjects with MS showed significant increases in CACS and progression of CAD compared with counterparts without MS, in parallel with the numbers of MS components. Finally, MS was a significant predictor for the progression of CACS (hazard ratio 1.32; 95 % confidence interval 1.06–1.64) and progression of coronary artery stenosis and/or development of vulnerable plaque (hazard ratio 1.47, 95 % confidence interval 1.01–2.15) after adjusting for other cardiovascular risk factors. Subjects with MS showed progression of CAD as assessed by CACS and CCTA over ~3 years. Therefore, more vigilant screening for coronary vascular health is needed among those with MS.

31 December 2021 in Endocrinology and Metabolism
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Journal Article
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YKYe An Kim
Ye An Kim
JYJi Won Yoon
Ji Won Yoon
YLYoung Lee
Young Lee
HCHyuk Jin Choi
Hyuk Jin Choi
JYJae Won Yun
Jae Won Yun
JSJe Hyun Seo
Je Hyun Seo
Background: Epidemiological data have shown that vitamin D deficiency is highly prevalent in Korea. Genetic factors influencing vitamin D deficiency in humans have been studied in Europe but are less known in East Asian countries, including Korea. We aimed to investigate the genetic factors related to vitamin D levels in Korean people using a genome-wide association study (GWAS).Methods: We included 12,642 subjects from three different genetic cohorts consisting of Korean participants. The GWAS was performed on 7,590 individuals using linear or logistic regression meta- and mega-analyses. After identifying significant single nucleotide polymorphisms (SNPs), we calculated heritability and performed replication and rare variant analyses. In addition, expression quantitative trait locus (eQTL) analysis for significant SNPs was performed.Results: rs12803256, in the actin epsilon 1, pseudogene (ACTE1P) gene, was identified as a novel polymorphism associated with vitamin D deficiency. SNPs, such as rs11723621 and rs7041, in the group-specific component gene (GC) and rs11023332 in the phosphodiesterase 3B (PDE3B) gene were significantly associated with vitamin D deficiency in both meta- and mega-analyses. The SNP heritability of the vitamin D concentration was estimated to be 7.23%. eQTL analysis for rs12803256 for the genes related to vitamin D metabolism, including glutamine-dependent NAD(+) synthetase (NADSYN1) and 7-dehydrocholesterol reductase (DHCR7), showed significantly different expression according to alleles.Conclusion: The genetic factors underlying vitamin D deficiency in Korea included polymorphisms in the GC, PDE3B, NADSYN1, and ACTE1P genes. The biological mechanism of a non-coding SNP (rs12803256) for DHCR7/NADSYN1 on vitamin D concentrations is unclear, warranting further investigations.