Dankyu Yoon
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Research Subjects
Dankyu Yoon has a total of 53 co-authors. Here are the top co-authors by number of shared publications:
- Chol Shin
Institute of Human Genomic Study, College of Medicine, Korea University Ansan Hospital, Republic of Korea
2 shared publications - Joo Hyun Lim
Division of Endocrine and Kidney Disease Research, Department of Chronic Disease Convergence Research, National Institute of Health, Cheongju 28159, Republic of Korea
2 shared publications - Soriul Kim
Department of Preventive Medicine, College and School of Medicine, Kangwon National University, Chuncheon, Republic of Korea
2 shared publications - Sungho Won
Institute of Health and Environment, Seoul National University, Seoul, Republic of Korea
2 shared publications - Woo Jin Kim
Department of Internal Medicine and Environmental Health Center, Kangwon National University, Chuncheon, Republic of Korea
2 shared publications - Ah Ra Do
Interdisciplinary Program of Bioinformatics, Seoul National University, Seoul 08826, Korea
1 shared publication
Latest Publications
- Open Access
Sex-Specific Associations of Childhood BMI Patterns with Cardiometabolic Risk: An 11-Year Korean Longitudinal Study
Background/Objectives: Childhood overweight/obesity status is a critical risk factor for adverse cardiometabolic outcomes. We aimed to evaluate the sex-specific associations between a maintained childhood overweight status and late-adolescent cardiometabolic risk factors using data from a Korean longitudinal study. Methods: We used data from the Korean Children-Adolescents Study, a prospective cohort of children enrolled at age 7 and followed annually from 2005 to 2020. Among participants who were followed at least once, a total of 899 children (438 boys, 461 girls) with consistent body mass index (BMI) status at ages 7–9 and 10–12 were included in the analysis. Participants were categorized into two groups on the basis of BMI: normal weight maintenance and overweight maintenance. Multivariable linear regression was used to examine the associations between BMI patterns and cardiometabolic risk factors, with adjustments for covariates. Results: Among the 899 children (mean age: 7.1 ± 0.4 years, 48.7% boys), 12.8% of boys and 5.9% of girls were classified into the overweight maintenance group. Boys in the overweight maintenance group had significantly greater BMIs, waist circumferences (WC), body fat percentages, trunk fat mass, and aspartate aminotransferase and alanine aminotransferase levels at ages 15 and 18. Girls in the same group had elevated BMI, WC, body fat percentage, trunk fat mass, and blood pressure and experienced earlier pubertal onset. Conclusions: Maintaining an overweight status during childhood is associated with adverse cardiometabolic profiles in adolescence, with sex-specific differences. These findings highlight the importance of early, sex-specific interventions to prevent long-term health risks associated with childhood obesity.
Open AccessSex-Specific Associations of Childhood BMI Patterns with Cardiometabolic Risk: An 11-Year Korean Longitudinal Study
Background/Objectives: Childhood overweight/obesity status is a critical risk factor for adverse cardiometabolic outcomes. We aimed to evaluate the sex-specific associations between a maintained childhood overweight status and late-adolescent cardiometabolic risk factors using data from a Korean longitudinal study. Methods: We used data from the Korean Children-Adolescents Study, a prospective cohort of children enrolled at age 7 and followed annually from 2005 to 2020. Among participants who were followed at least once, a total of 899 children (438 boys, 461 girls) with consistent body mass index (BMI) status at ages 7–9 and 10–12 were included in the analysis. Participants were categorized into two groups on the basis of BMI: normal weight maintenance and overweight maintenance. Multivariable linear regression was used to examine the associations between BMI patterns and cardiometabolic risk factors, with adjustments for covariates. Results: Among the 899 children (mean age: 7.1 ± 0.4 years, 48.7% boys), 12.8% of boys and 5.9% of girls were classified into the overweight maintenance group. Boys in the overweight maintenance group had significantly greater BMIs, waist circumferences (WC), body fat percentages, trunk fat mass, and aspartate aminotransferase and alanine aminotransferase levels at ages 15 and 18. Girls in the same group had elevated BMI, WC, body fat percentage, trunk fat mass, and blood pressure and experienced earlier pubertal onset. Conclusions: Maintaining an overweight status during childhood is associated with adverse cardiometabolic profiles in adolescence, with sex-specific differences. These findings highlight the importance of early, sex-specific interventions to prevent long-term health risks associated with childhood obesity.
- Open Access
Association Between Ultraprocessed Food Consumption and Metabolic Disorders in Children and Adolescents with Obesity
Background/Objectives: We investigated the effects of ultraprocessed food (UPF) consumption on metabolic disorders (e.g., adiposity, metabolic associated steatotic liver disease [MASLD], and insulin resistance) in children and adolescents with obesity to improve dietary guidelines and public health strategies. Methods: The dietary intake of 149 participants (aged 8–17 years) was assessed with food diaries. The NOVA classification system was used to classify food according to the degree of processing. Metabolic outcomes, including the fat mass index (FMI), hepatic fat percentage, and insulin resistance, were measured via dual-energy X-ray absorptiometry (DXA), magnetic resonance imaging proton density fat fraction (MRI-PDFF), and biochemical analysis, respectively. Results: Greater UPF consumption from baseline to the 6-month follow-up was significantly associated with increased insulin and decreased total cholesterol and LDL-cholesterol. UPF consumption was positively associated with the prevalence of MASLD (liver MRI-PDFF ≥ 5%; odds ratio T3 vs. T1 = 1.75; 95% confidence interval [CI] 1.03, 3.00), moderate-to-severe MASLD (liver MRI-PDFF ≥ 10%; OR T3 vs. T1 = 4.19; 95% CI 1.72, 10.22), and insulin resistance (OR T3 vs. T1 = 2.44; 95% CI 1.33, 4.48), after adjusting for covariates. A linear dose-response relationship was observed between UPF consumption and the odds of moderate-to-severe MASLD and insulin resistance. Conclusions: Greater UPF consumption was strongly associated with MASLD and insulin resistance in children and adolescents with obesity, underscoring the importance of reducing UPF consumption through dietary guidelines and public health interventions to mitigate the risk of obesity-related metabolic conditions in young populations.
Open AccessAssociation Between Ultraprocessed Food Consumption and Metabolic Disorders in Children and Adolescents with Obesity
Background/Objectives: We investigated the effects of ultraprocessed food (UPF) consumption on metabolic disorders (e.g., adiposity, metabolic associated steatotic liver disease [MASLD], and insulin resistance) in children and adolescents with obesity to improve dietary guidelines and public health strategies. Methods: The dietary intake of 149 participants (aged 8–17 years) was assessed with food diaries. The NOVA classification system was used to classify food according to the degree of processing. Metabolic outcomes, including the fat mass index (FMI), hepatic fat percentage, and insulin resistance, were measured via dual-energy X-ray absorptiometry (DXA), magnetic resonance imaging proton density fat fraction (MRI-PDFF), and biochemical analysis, respectively. Results: Greater UPF consumption from baseline to the 6-month follow-up was significantly associated with increased insulin and decreased total cholesterol and LDL-cholesterol. UPF consumption was positively associated with the prevalence of MASLD (liver MRI-PDFF ≥ 5%; odds ratio T3 vs. T1 = 1.75; 95% confidence interval [CI] 1.03, 3.00), moderate-to-severe MASLD (liver MRI-PDFF ≥ 10%; OR T3 vs. T1 = 4.19; 95% CI 1.72, 10.22), and insulin resistance (OR T3 vs. T1 = 2.44; 95% CI 1.33, 4.48), after adjusting for covariates. A linear dose-response relationship was observed between UPF consumption and the odds of moderate-to-severe MASLD and insulin resistance. Conclusions: Greater UPF consumption was strongly associated with MASLD and insulin resistance in children and adolescents with obesity, underscoring the importance of reducing UPF consumption through dietary guidelines and public health interventions to mitigate the risk of obesity-related metabolic conditions in young populations.
- Open Access
Heritability Analyses Uncover Shared Genetic Effects of Lung Function and Change over Time
Genetic influence on lung functions has been identified in previous studies; however, the relative longitudinal effects of genetic factors and their interactions with smoking on lung function remain unclear. Here, we identified the longitudinal effects of genetic variants on lung function by determining single nucleotide polymorphism (SNP) heritability and genetic correlations, and by analyzing interactions with smoking. Subject-specific means and annual change rates were calculated for eight spirometric measures obtained from 6622 Korean adults aged 40–69 years every two years for 14 years, and their heritabilities were estimated separately. Statistically significant (p < 0.05) heritability for the subject-specific means of all spirometric measures (8~32%) and change rates of forced expiratory volume in 1 s to forced vital capacity ratio (FEV1/FVC; 16%) and post-bronchodilator FEV1/FVC (17%) were detected. Significant genetic correlations of the change rate with the subject-specific mean were observed for FEV1/FVC ( = 0.64) and post-bronchodilator FEV1/FVC ( = 0.47). Furthermore, post-bronchodilator FEV1/FVC showed significant heritability of SNP-by-smoking interaction ( = 0.4) for the annual change rate. The GWAS also detected genome-wide significant SNPs for FEV1 (rs4793538), FEV1/FVC (rs2704589, rs62201158, and rs9391733), and post-bronchodilator FEV1/FVC (rs2445936). We found statistically significant evidence of heritability role on the change in lung function, and this was shared with the effects on cross-sectional measurements. We also found some evidence of interaction with smoking for the change of lung function.Open AccessHeritability Analyses Uncover Shared Genetic Effects of Lung Function and Change over Time
Genetic influence on lung functions has been identified in previous studies; however, the relative longitudinal effects of genetic factors and their interactions with smoking on lung function remain unclear. Here, we identified the longitudinal effects of genetic variants on lung function by determining single nucleotide polymorphism (SNP) heritability and genetic correlations, and by analyzing interactions with smoking. Subject-specific means and annual change rates were calculated for eight spirometric measures obtained from 6622 Korean adults aged 40–69 years every two years for 14 years, and their heritabilities were estimated separately. Statistically significant (p < 0.05) heritability for the subject-specific means of all spirometric measures (8~32%) and change rates of forced expiratory volume in 1 s to forced vital capacity ratio (FEV1/FVC; 16%) and post-bronchodilator FEV1/FVC (17%) were detected. Significant genetic correlations of the change rate with the subject-specific mean were observed for FEV1/FVC ( = 0.64) and post-bronchodilator FEV1/FVC ( = 0.47). Furthermore, post-bronchodilator FEV1/FVC showed significant heritability of SNP-by-smoking interaction ( = 0.4) for the annual change rate. The GWAS also detected genome-wide significant SNPs for FEV1 (rs4793538), FEV1/FVC (rs2704589, rs62201158, and rs9391733), and post-bronchodilator FEV1/FVC (rs2445936). We found statistically significant evidence of heritability role on the change in lung function, and this was shared with the effects on cross-sectional measurements. We also found some evidence of interaction with smoking for the change of lung function. - Open Access
Genome-Wide Association Study of Airway Wall Thickening in a Korean Chronic Obstructive Pulmonary Disease Cohort
Airway wall thickening (AWT) plays an important pathophysiological role in airway diseases such as chronic obstructive pulmonary disease (COPD). There are only a few studies on the genetic components contributing to AWT in the Korean population. This study aimed to identify AWT-related single-nucleotide polymorphisms (SNPs) using a genome-wide association study (GWAS). We performed GWAS for AWT using the CODA and KUCOPD cohorts. Thereafter, a meta-analysis was performed. Airway wall thickness was measured using automatic segmentation software. The AWT at an internal perimeter of 10 mm (AWT-Pi10) was calculated by the square root of the theoretical airway wall area using the full-width-half-maximum method. We identified a significant SNP (rs11648772, p = 1.41 × 10−8) located in LINC02127, near SALL1. This gene is involved in the inhibition of epithelial–mesenchymal transition in glial cells, and it affects bronchial wall depression in COPD patients. Additionally, we identified other SNPs (rs11970854, p = 1.92 × 10−6; rs16920168, p = 5.29 × 10−6) involved in airway inflammation and proliferation and found that AWT is influenced by these genetic variants. Our study helps identify the genetic cause of COPD in an Asian population and provides a potential basis for treatment.
Open AccessGenome-Wide Association Study of Airway Wall Thickening in a Korean Chronic Obstructive Pulmonary Disease Cohort
Airway wall thickening (AWT) plays an important pathophysiological role in airway diseases such as chronic obstructive pulmonary disease (COPD). There are only a few studies on the genetic components contributing to AWT in the Korean population. This study aimed to identify AWT-related single-nucleotide polymorphisms (SNPs) using a genome-wide association study (GWAS). We performed GWAS for AWT using the CODA and KUCOPD cohorts. Thereafter, a meta-analysis was performed. Airway wall thickness was measured using automatic segmentation software. The AWT at an internal perimeter of 10 mm (AWT-Pi10) was calculated by the square root of the theoretical airway wall area using the full-width-half-maximum method. We identified a significant SNP (rs11648772, p = 1.41 × 10−8) located in LINC02127, near SALL1. This gene is involved in the inhibition of epithelial–mesenchymal transition in glial cells, and it affects bronchial wall depression in COPD patients. Additionally, we identified other SNPs (rs11970854, p = 1.92 × 10−6; rs16920168, p = 5.29 × 10−6) involved in airway inflammation and proliferation and found that AWT is influenced by these genetic variants. Our study helps identify the genetic cause of COPD in an Asian population and provides a potential basis for treatment.
- Open Access
- 26 October 2020
- Published by Springer Nature in Journal of Human Genetics
- Vol. 66 (5) , 475-489
Association of an IGHV3-66 gene variant with Kawasaki disease
In a meta-analysis of three GWAS for susceptibility to Kawasaki disease (KD) conducted in Japan, Korea, and Taiwan and follow-up studies with a total of 11,265 subjects (3428 cases and 7837 controls), a significantly associated SNV in the immunoglobulin heavy variable gene (IGHV) cluster in 14q33.32 was identified (rs4774175; OR = 1.20, P = 6.0 × 10−9). Investigation of nonsynonymous SNVs of the IGHV cluster in 9335 Japanese subjects identified the C allele of rs6423677, located in IGHV3-66, as the most significant reproducible association (OR = 1.25, P = 6.8 × 10−10 in 3603 cases and 5731 controls). We observed highly skewed allelic usage of IGHV3-66, wherein the rs6423677 A allele was nearly abolished in the transcripts in peripheral blood mononuclear cells of both KD patients and healthy adults. Association of the high-expression allele with KD strongly indicates some active roles of B-cells or endogenous immunoglobulins in the disease pathogenesis. Considering that significant association of SNVs in the IGHV region with disease susceptibility was previously known only for rheumatic heart disease (RHD), a complication of acute rheumatic fever (ARF), these observations suggest that common B-cell related mechanisms may mediate the symptomology of KD and ARF as well as RHD.
- 26 October 2020
- Published by Springer Nature in Journal of Human Genetics
- Vol. 66 (5) , 475-489
Open AccessAssociation of an IGHV3-66 gene variant with Kawasaki disease
In a meta-analysis of three GWAS for susceptibility to Kawasaki disease (KD) conducted in Japan, Korea, and Taiwan and follow-up studies with a total of 11,265 subjects (3428 cases and 7837 controls), a significantly associated SNV in the immunoglobulin heavy variable gene (IGHV) cluster in 14q33.32 was identified (rs4774175; OR = 1.20, P = 6.0 × 10−9). Investigation of nonsynonymous SNVs of the IGHV cluster in 9335 Japanese subjects identified the C allele of rs6423677, located in IGHV3-66, as the most significant reproducible association (OR = 1.25, P = 6.8 × 10−10 in 3603 cases and 5731 controls). We observed highly skewed allelic usage of IGHV3-66, wherein the rs6423677 A allele was nearly abolished in the transcripts in peripheral blood mononuclear cells of both KD patients and healthy adults. Association of the high-expression allele with KD strongly indicates some active roles of B-cells or endogenous immunoglobulins in the disease pathogenesis. Considering that significant association of SNVs in the IGHV region with disease susceptibility was previously known only for rheumatic heart disease (RHD), a complication of acute rheumatic fever (ARF), these observations suggest that common B-cell related mechanisms may mediate the symptomology of KD and ARF as well as RHD.