Effect of the Interaction between Seaweed Intake and LPL Polymorphisms on Metabolic Syndrome in Middle-Aged Korean Adults.

This study aimed to examine the effect of the interaction between seaweed (laver, kelp, and sea mustard) intake and lipoprotein lipase gene (LPL) rs17482735 genotypes on the incidence of metabolic syndrome (MetS). The Korean Genome and Epidemiology Study (KoGES) data of Korean adults aged 40-69 years were used in this study. Information on seaweed intake was obtained from the food frequency questionnaire. To investigate the interaction between seaweed intake and LPL rs17482735 genotypes on the incidence of MetS, multivariable Cox proportional hazard models were used after adjusting for confounding variables. There was no significant association in women, but men with TG and TT genotypes of rs17482753 had lower incidence of MetS (HR 0.83, 95% CI 0.71-0.95, p-value = 0.01), low HDL-cholesterol levels (HR 0.81, 95% CI 0.69-0.95, p-value = 0.01), high triglyceride levels (HR 0.83, 95% CI 0.70-0.99, p-value = 0.0471), and high blood pressure (HR 0.79, 95% CI 0.67-0.93, p-value = 0.004). Furthermore, the incidence of MetS was lower in men with the highest laver and total seaweed intake and TG and TT genotypes of rs17482735 (HR 0.60, 95% CI 0.43-0.84; HR 0.57, 95% CI 0.41-0.79, respectively). High seaweed intake was negatively associated with MetS, suggesting that LPL genetic variations, particularly in men, may be helpful in preventing MetS. These results demonstrate that seaweed intake considering LPL genotypes may be beneficial for preventing and treating MetS.

How Do Brown Seaweeds Work on Biomarkers of Dyslipidemia? A Systematic Review with Meta-Analysis and Meta-Regression.

Dyslipidemia is a common chronic disease that increases the risk of cardiovascular disease. Diet plays an important role in the development of dyslipidemia. As people pay increased attention to healthy eating habits, brown seaweed consumption is increasing, particularly in East Asian countries. The association between dyslipidemia and brown seaweed consumption has been previously demonstrated. We searched for keywords associated with brown seaweed and dyslipidemia in electronic databases such as PubMed, Embase, and Cochrane. Heterogeneity was estimated using the I2 statistic. The 95% confidence interval (CI) of the forest plot and heterogeneity were confirmed using meta-ANOVA and meta-regression. Funnel plots and publication bias statistical tests were used to determine publication bias. Statistical significance was set at p < 0.05. In this meta-analysis, we found that brown seaweed intake significantly decreased the levels of total cholesterol (mean difference (MD): -3.001; 95% CI: -5.770, -0.232) and low-density lipoprotein (LDL) cholesterol (MD: -6.519; 95% CI: -12.884, -0.154); nevertheless, the statistically significant association of brown seaweed intake with high-density lipoprotein (HDL) cholesterol and triglycerides were not observed in our study (MD: 0.889; 95% CI: -0.558, 2.335 and MD: 8.515; 95% CI: -19.354, 36.383). Our study demonstrated that brown seaweed and its extracts decreased total cholesterol and LDL cholesterol levels. The use of brown seaweeds may be a promising strategy to reduce the risk of dyslipidemia. Future studies involving a larger population are warranted to investigate the dose-response association of brown seaweed consumption with dyslipidemia.

Identification of genetic variants related to metabolic syndrome by next-generation sequencing.

BACKGROUND: Metabolic syndrome (MetS) is a cluster of conditions associated with glucose intolerance, hypertension, abdominal obesity, dyslipidemia, and insulin resistance that increase the risk of cardiovascular diseases (CVD) and type 2 diabetes (T2D). Since MetS is known as a complex symptom with a high incidence of genetic factors, it is important to identify genetic variants for each clinical characteristic of MetS. METHODS: We performed targeted next-generation sequencing (NGS) to identify genetic variants related to obesity, blood glucose, triacylglycerol (TG), and high-density lipoprotein (HDL)-cholesterol level, and hypertension in 48 subjects with MetS and in 48 healthy subjects. RESULTS: NGS analysis revealed that 26 of 48 subjects (54.2%) with MetS had putative non-synonymous variants related to the clinical features of MetS. Of the subjects with MetS, 8 (16.7%) had variants in 4 genes (COL6A2, FTO, SPARC, and MTHFR) related to central obesity, 17 (35.4%) had variants in 6 genes (APOB, SLC2A2, LPA, ABCG5, ABCG8, and GCKR) related to hyperglycemia, 3 (6.3%) had variants in 4 genes (APOA1, APOC2, APOA4, and LMF1) related to hypertriglyceridemia, 8 (16.7%) had variants in 4 genes (ABCA1, CETP, SCARB1, and LDLR) related to low HDL-cholesterolemia, and 5 (10.4%) had variants in ADD1 related to hypertension. CONCLUSIONS: Our findings may contribute to broadening the genetic spectrum of risk variants related to the development of MetS.

Genetic Variants Associated with Elevated Plasma Ceramides in Individuals with Metabolic Syndrome.

Metabolic syndrome (MetS) is a complex condition of metabolic disorders and shows a steady onset globally. Ceramides are known as intracellular signaling molecules that influence key metabolism through various pathways such as MetS and insulin resistance. Therefore, it is important to identify novel genetic factors related to increased plasma ceramides in subjects with MetS. Here we first measured plasma ceramides levels in 37 subjects with MetS and in 38 healthy subjects by ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS). Specifically, levels of C16 ceramide (Cer-16), C18 ceramide (Cer-18), C20 ceramide (Cer-20), C18 dihydroceramide (DhCer-18), C24 dihydroceramide (DhCer-24), and C24:1 dihydroceramide (DhCer-24:1) were significantly increased in MetS group (p < 5.0 × 10−2). We then performed single nucleotide polymorphism (SNP) genotyping to identify variants associated with elevated plasma ceramides in MetS group using Axiom® Korea Biobank Array v1.1 chip. We also performed linear regression analysis on genetic variants involved in ceramide synthesis and significantly elevated plasma ceramides and dihydroceramides. Ten variants (rs75397325, rs4246316, rs80165332, rs62106618, rs12358192, rs11006229, rs10826014, rs149162405, rs6109681, and rs3906631) across six genes (ACER1, CERS3, CERS6, SGMS1, SPTLC2, and SPTLC3) functionally involved in ceramide biosynthesis showed significant associations with the elevated levels of at least one of the ceramide species in MetS group at a statistically significant threshold of false discovery rate (FDR)-adjusted p < 5.0 × 10−2. Our findings suggest that the variants may be genetic determinants associated with increased plasma ceramides in individuals with MetS.

Comparative analysis of mutational hotspots in the spike protein of SARS-CoV-2 isolates from different geographic origins.

The spike (S) protein mutations of SARS-CoV-2 are of major concern in terms of viral transmission and pathogenesis. Hence, we developed a PCR-based method to rapidly detect the 6 mutational hotspots (H49Y, G476S, V483A, H519Q, A520S, and D614G) in the S protein and applied this method to analyze the hotspots in the viral isolates from different geographical origins. Here, we identified that there was only the D614G mutation in the viral isolates. As of September 30, 2020, the analysis of 113,381 sequences available from the public repositories revealed that the SARS-CoV-2 variant carrying G614 has become the most prevalent form globally. Our results support recent epidemiological and genomic data demonstrating that the viral infectivity and transmission are enhanced by the S protein D614G mutation.