Purpose: Metabolic syndrome (MetS) is a condition in which multiple risk factors interact in a complex manner. Considerable attention has been directed towards the potential genetic contributions to its diverse mechanisms. Understanding these contributions is essential for reducing MetS and other chronic diseases and developing effective prevention strategies.Therefore, this study analyzed the research trends in academic papers exploring genetic factors related to MetS and its components in Koreans and attempted to identify areas requiring additional research. Methods: The scoping review method was used to evaluate studies that utilized the secondary data sets comprising the Korean Genome and Epidemiology Study. Articles published over the past 15 years were identified using the Research Information Sharing Service, Korean Studies Information Service System, DBpia, PubMed, and ScienceDirect databases. Results: Forty-seven published articles from 2010 to 2024 were included in the review.Research on the genetic factors linked to MetS has expanded since 2019, indicating significant advances in the field. The research included 18 studies on the polygenic risk score (PRS)/genetic risk score (GRS), 17 studies on single nucleotide polymorphisms (SNPs), six studies on two or more genes, four studies on DNA methylation, and two studies on copy number variations (CNVs). In PRS/GRS research, seven studies focused on the genes related to diseases. In SNP research, four studies examined the FTO gene. Studies on two or more genes included two studies, each on the genes associated with diabetes and high-density lipoprotein cholesterol. For DNA methylation, three studies focused on the TXNIP gene. Finally, in CNV research, one study was conducted on the LEPR gene and one on genes for hypertension. Conclusion The relatively low proportion of studies on DNA methylation and CNV presents limitations in understanding their associations with MetS. Expanded research utilizing diverse approaches and genetic variables is needed to overcome these limitations.

Purpose: Metabolic syndrome (MetS) is a condition in which multiple risk factors interact in a complex manner. Considerable attention has been directed towards the potential genetic contributions to its diverse mechanisms. Understanding these contributions is essential for reducing MetS and other chronic diseases and developing effective prevention strategies.Therefore, this study analyzed the research trends in academic papers exploring genetic factors related to MetS and its components in Koreans and attempted to identify areas requiring additional research. Methods: The scoping review method was used to evaluate studies that utilized the secondary data sets comprising the Korean Genome and Epidemiology Study. Articles published over the past 15 years were identified using the Research Information Sharing Service, Korean Studies Information Service System, DBpia, PubMed, and ScienceDirect databases. Results: Forty-seven published articles from 2010 to 2024 were included in the review.Research on the genetic factors linked to MetS has expanded since 2019, indicating significant advances in the field. The research included 18 studies on the polygenic risk score (PRS)/genetic risk score (GRS), 17 studies on single nucleotide polymorphisms (SNPs), six studies on two or more genes, four studies on DNA methylation, and two studies on copy number variations (CNVs). In PRS/GRS research, seven studies focused on the genes related to diseases. In SNP research, four studies examined the FTO gene. Studies on two or more genes included two studies, each on the genes associated with diabetes and high-density lipoprotein cholesterol. For DNA methylation, three studies focused on the TXNIP gene. Finally, in CNV research, one study was conducted on the LEPR gene and one on genes for hypertension. Conclusion The relatively low proportion of studies on DNA methylation and CNV presents limitations in understanding their associations with MetS. Expanded research utilizing diverse approaches and genetic variables is needed to overcome these limitations.

Purpose: Metabolic syndrome (MetS) is a condition in which multiple risk factors interact in a complex manner. Considerable attention has been directed towards the potential genetic contributions to its diverse mechanisms. Understanding these contributions is essential for reducing MetS and other chronic diseases and developing effective prevention strategies.Therefore, this study analyzed the research trends in academic papers exploring genetic factors related to MetS and its components in Koreans and attempted to identify areas requiring additional research. Methods: The scoping review method was used to evaluate studies that utilized the secondary data sets comprising the Korean Genome and Epidemiology Study. Articles published over the past 15 years were identified using the Research Information Sharing Service, Korean Studies Information Service System, DBpia, PubMed, and ScienceDirect databases. Results: Forty-seven published articles from 2010 to 2024 were included in the review.Research on the genetic factors linked to MetS has expanded since 2019, indicating significant advances in the field. The research included 18 studies on the polygenic risk score (PRS)/genetic risk score (GRS), 17 studies on single nucleotide polymorphisms (SNPs), six studies on two or more genes, four studies on DNA methylation, and two studies on copy number variations (CNVs). In PRS/GRS research, seven studies focused on the genes related to diseases. In SNP research, four studies examined the FTO gene. Studies on two or more genes included two studies, each on the genes associated with diabetes and high-density lipoprotein cholesterol. For DNA methylation, three studies focused on the TXNIP gene. Finally, in CNV research, one study was conducted on the LEPR gene and one on genes for hypertension. Conclusion The relatively low proportion of studies on DNA methylation and CNV presents limitations in understanding their associations with MetS. Expanded research utilizing diverse approaches and genetic variables is needed to overcome these limitations.

Purpose: Metabolic diseases share common risk factors, requiring the development of therapeutic agents with multi-target effects. Although the ameliorating effects of Porphyra tenera ethanol extract (PTE) have been reported on some individual metabolic disorders, studies addressing various other metabolic diseases are still limited. This study investigated the ameliorating effects of PTE supplementation for 12 weeks on obesity, dyslipidemia, and hepatic lipid metabolism in high-fat diet (HFD)-induced obese mice and its molecular mechanisms. Methods: Male C57BL/6 mice (n = 12/in each group) were divided into six groups for 12 weeks: control, HFD, chow diet + 1% porphyran, chow diet + 4% porphyran, HFD + 1% porphyran (HPYP-L), and HFD + 4% porphyran (HPYP-H). To confirm the attenuation of metabolic disease in vivo, mice in the HFD, HPYP-L and HPYP-H groups were fed 60% HFD to induce obesity. PTE was prepared using ethanol and dissolved in drinking water to concentrations of 1% and 4% porphyran. After 12 weeks of free PTE intake, body weight measurement, serum analysis, histopathological analysis, real-time quantitative polymerase chain reaction, and Western blot analysis of liver tissues were performed for comparative evaluation. Results: After 12 weeks, the HPYP-L and HPYP-H groups showed a decreased body weight, improved blood lipids, and reduced hepatic lipid droplet accumulation vs. the HFD group.Liver acetyl-CoA carboxylase, was suppressed in the HPYP-L group vs. the HFD group.The B-cell lymphoma 2 (Bcl-2)-associated X protein/Bcl-2 protein and messenger RNA (mRNA) level ratio in the liver decreased after PTE intake, indicating inhibition of apoptosis.Interleukin-1 beta mRNA expression in the liver was reduced in the HPYP-L group vs. the HFD group. In the liver, lower protein carbonylation levels in the HPYP-H group indicated reduced oxidative stress, while the increased mitochondrial DNAuclear DNA ratio indicated improved mitochondrial function. Conclusion PTE protects against diet-induced metabolic disorders and could be a potential agent for the prevention and treatment of metabolic diseases.

Purpose: Metabolic diseases share common risk factors, requiring the development of therapeutic agents with multi-target effects. Although the ameliorating effects of Porphyra tenera ethanol extract (PTE) have been reported on some individual metabolic disorders, studies addressing various other metabolic diseases are still limited. This study investigated the ameliorating effects of PTE supplementation for 12 weeks on obesity, dyslipidemia, and hepatic lipid metabolism in high-fat diet (HFD)-induced obese mice and its molecular mechanisms. Methods: Male C57BL/6 mice (n = 12/in each group) were divided into six groups for 12 weeks: control, HFD, chow diet + 1% porphyran, chow diet + 4% porphyran, HFD + 1% porphyran (HPYP-L), and HFD + 4% porphyran (HPYP-H). To confirm the attenuation of metabolic disease in vivo, mice in the HFD, HPYP-L and HPYP-H groups were fed 60% HFD to induce obesity. PTE was prepared using ethanol and dissolved in drinking water to concentrations of 1% and 4% porphyran. After 12 weeks of free PTE intake, body weight measurement, serum analysis, histopathological analysis, real-time quantitative polymerase chain reaction, and Western blot analysis of liver tissues were performed for comparative evaluation. Results: After 12 weeks, the HPYP-L and HPYP-H groups showed a decreased body weight, improved blood lipids, and reduced hepatic lipid droplet accumulation vs. the HFD group.Liver acetyl-CoA carboxylase, was suppressed in the HPYP-L group vs. the HFD group.The B-cell lymphoma 2 (Bcl-2)-associated X protein/Bcl-2 protein and messenger RNA (mRNA) level ratio in the liver decreased after PTE intake, indicating inhibition of apoptosis.Interleukin-1 beta mRNA expression in the liver was reduced in the HPYP-L group vs. the HFD group. In the liver, lower protein carbonylation levels in the HPYP-H group indicated reduced oxidative stress, while the increased mitochondrial DNAuclear DNA ratio indicated improved mitochondrial function. Conclusion PTE protects against diet-induced metabolic disorders and could be a potential agent for the prevention and treatment of metabolic diseases.

Purpose: Metabolic diseases share common risk factors, requiring the development of therapeutic agents with multi-target effects. Although the ameliorating effects of Porphyra tenera ethanol extract (PTE) have been reported on some individual metabolic disorders, studies addressing various other metabolic diseases are still limited. This study investigated the ameliorating effects of PTE supplementation for 12 weeks on obesity, dyslipidemia, and hepatic lipid metabolism in high-fat diet (HFD)-induced obese mice and its molecular mechanisms. Methods: Male C57BL/6 mice (n = 12/in each group) were divided into six groups for 12 weeks: control, HFD, chow diet + 1% porphyran, chow diet + 4% porphyran, HFD + 1% porphyran (HPYP-L), and HFD + 4% porphyran (HPYP-H). To confirm the attenuation of metabolic disease in vivo, mice in the HFD, HPYP-L and HPYP-H groups were fed 60% HFD to induce obesity. PTE was prepared using ethanol and dissolved in drinking water to concentrations of 1% and 4% porphyran. After 12 weeks of free PTE intake, body weight measurement, serum analysis, histopathological analysis, real-time quantitative polymerase chain reaction, and Western blot analysis of liver tissues were performed for comparative evaluation. Results: After 12 weeks, the HPYP-L and HPYP-H groups showed a decreased body weight, improved blood lipids, and reduced hepatic lipid droplet accumulation vs. the HFD group.Liver acetyl-CoA carboxylase, was suppressed in the HPYP-L group vs. the HFD group.The B-cell lymphoma 2 (Bcl-2)-associated X protein/Bcl-2 protein and messenger RNA (mRNA) level ratio in the liver decreased after PTE intake, indicating inhibition of apoptosis.Interleukin-1 beta mRNA expression in the liver was reduced in the HPYP-L group vs. the HFD group. In the liver, lower protein carbonylation levels in the HPYP-H group indicated reduced oxidative stress, while the increased mitochondrial DNAuclear DNA ratio indicated improved mitochondrial function. Conclusion PTE protects against diet-induced metabolic disorders and could be a potential agent for the prevention and treatment of metabolic diseases.

Background: There is limited evidence on the safety of coronavirus disease 2019 (COVID-19) vaccination during pregnancy and lactation. Thus, we aimed to evaluate the association between COVID-19 vaccination during pregnancy and lactation and reporting risk of adverse pregnancy or lactation outcomes. Methods: Using VigiBase, we performed a disproportionality analysis with caseon case design. Cases were defined based on the Standardized MedDRA Queries (SMQs) of “pregnancy and neonatal topics” and non-cases were defined as all other adverse events. We included all reports with COVID-19 vaccines as the suspected cause. Using the full database as the comparators, reporting odds ratios (RORs) with 95% confidence intervals (CIs) were estimated by logistic regression while adjusting for maternal age. Infants’ age and sex were additionally adjusted in analyzing the risk of COVID-19 vaccination during lactation. Results: We identified 10,266 and 6,474 reports with the SMQ of “pregnancy and neonatal topics” associated with COVID-19 vaccines during pregnancy and lactation, respectively. No significant RORs of adverse pregnancy outcomes associated with COVID-19 vaccines during pregnancy were observed; however, “functional lactation disorders” showed significant disproportionality during lactation with adjusted ROR of 1.48 (95% CI, 1.21–1.79). Further analysis that analyzed “functional lactation disorders” at a preferred term level, showed higher ROR in mastitis (2.76 [95% CI, 1.45–5.27]). Conclusion Overall, we did not observe a positive association between COVID-19 vaccination during pregnancy and risk of reporting adverse pregnancy outcomes. However, we found a significant disproportionate reporting association between COVID-19 vaccination during lactation and “functional lactation disorders”, specifically mastitis. Continuous surveillance is warranted to confirm the safety of COVID-19 vaccine during pregnancy and lactation.

Methods: Information on seaweed consumption was collected using a food frequency questionnaire, which included laver, kelp, and sea mustard among the items consumed. A total of 31 hs-CRP-related single nucleotide polymorphisms (SNPs) were selected using genomewide association studies and clumping analysis, and the individual PRS were calculated by weighting the effect size of each allele in the selected SNPs of 39,369 middle-aged (≥40 years) Koreans using the Korean Genome and Epidemiology Study (KoGES)-Health Examinees (HEXA) cohort data. To investigate the interaction between seaweed intake and the PRS on hs-CRP levels >1 mg/L, hazard ratios (HRs) and 95% confidence intervals (CIs) were assessed using multivariable Cox proportional hazards models. Results: During a mean follow-up period of 4.8 years, we recorded 436 patients with elevated hs-CRP levels. Women in the highest tertile of the PRS with the lowest quartile of seaweed intake had an increased incidence of elevated hs-CRP levels compared with women in the lowest tertile of the PRS with the lowest seaweed intake quartile (HR 2.34, 95% CI 1.23–4.45). No significant association was observed among the men. Conclusion In conclusion, we identified a new interaction between the PRS, seaweed intake, and inflammation in Korean women, and this study suggests that the interaction between the identification of genetic predisposition and dietary seaweed intake may have an impact on determining the risk of developing hyperinflammation in the future.

Purpose: High-sensitivity C-reactive protein (hs-CRP) is primarily synthesized in the liver upon stimulation of infectious disease cytokines, such as interleukin-6 (IL-6), and is used as a biological marker of systemic inflammation. Previous studies reported that hs-CRP is closely related to diet and abdominal obesity. Furthermore, a dietary score favoring the consumption of vegetables, fruits, and whole grains over meat and saturated fat reduced inflammation and decreased the prevalence of obesity and abdominal obesity. Nevertheless, no studies have examined whether hs-CRP mediates the relationship between dietary scores and abdominal obesity, and research on the Korean Healthy Eating Index (KHEI) is lacking. Therefore, the present study examined the association between the KHEI and abdominal obesity and the mediating effect of hs-CRP. Methods: In total, 17,770 adults aged ≥19 years were included in the study using the Korea National Health and Nutrition Examination Survey 2015–2018. KHEI was developed to assess the overall diet quality of Korean adults. Multivariable linear and logistic regression analyses assessed the relationship between KHEI, hs-CRP, and abdominal obesity. The mediation analysis with the bootstrapping method was performed using SAS MACRO. Results: Among women, the odds ratio (OR) of abdominal obesity prevalence was lower in the highest KHEI compared to the lowest KHEI after adjusting for age, body mass index, educational level, income level, occupational status, marital status, household type, region type, alcohol consumption, smoking status, physical activity, total energy intake, and hsCRP (OR 0.744, 95% confidence interval 0.598–0.926). The association between KHEI and abdominal obesity was partially mediated via hs-CRP, and the mediated proportion was 68.7% in men and 38.1% in women. Conclusion A substantial relationship was observed between the KHEI and abdominal obesity among females. Moreover, according to the KHEI, abdominal obesity may be mediated partially by hs-CRP.

BACKGROUND/OBJECTIVES: The high consumption of purine-rich meat is associated with hyperuricemia. However, there is limited evidence linking the consumption of red and processed meat to the genetic risk of hyperuricemia. We investigated the relationship between various combinations of red and processed meat consumption and the polygenic risk scores (PRSs) and the incidence of hyperuricemia in middle-aged Koreans. SUBJECTS/METHODS: We analyzed the data from 44,053 participants aged ≥40 years sourced from the Health Examinees (HEXA) cohort of the Korean Genome and Epidemiology Study (KoGES). Information regarding red and processed meat intake was obtained using a semiquantitative food frequency questionnaire (SQ-FFQ). We identified 69 independent single-nucleotide polymorphisms (SNPs) at uric acid-related loci using genome-wide association studies (GWASs) and clumping analyses. The individual PRS, which is the weighted sum of the effect size of each allele at the SNP, was calculated. We used multivariable Cox proportional hazards models adjusted for covariates to determine the relationship between red and processed meat intake and the PRS in the incidence of hyperuricemia. RESULTS: During an average follow-up period of 5 years, 2,556 patients with hyperuricemia were identified. For both men and women, the group with the highest red and processed meat intake and the highest PRS was positively associated with the development of hyperuricemia when compared with the group with the lowest red and processed meat intake and the lowest PRS (hazard ratio [HR], 2.72; 95% confidence interval [CI], 2.10–3.53; P < 0.0001; HR, 3.28; 95% CI, 2.45–4.40; P < 0.0001). CONCLUSION Individuals at a high genetic risk for uric acid levels should moderate their consumption of red and processed meat to prevent hyperuricemia.