RESUMEN
Vasoactive intrinsic peptide receptor (VIPR2), a circadian gene, is involved in metabolic homeostasis and metabolic syndrome (MetS). Seaweeds contain polysaccharides that regulate metabolic homeostasis, possibly by altering the effects of VIPR2 variants. We examined the relationship between VIPR2 expression and the incidence of MetS based on seaweed consumption. This study included 4979 Koreans aged ≥40 years using data from the Ansan-Ansung cohort of the Korean Genome and Epidemiology Study. The total seaweeds included were laver, kelp, and sea mustard. A multivariable Cox proportional hazards model was used to analyze the interactions between the VIPR2 rs6950857 genotype associated with MetS incidence and seaweed intake after adjusting for covariates such as region. A total of 2134 patients with MetS were followed for an average of 8.9 years. In men with the GG genotype of rs6950857, the highest quintile of seaweed consumption was associated with a decreased incidence of MetS compared with that of the lowest quintile (hazard ratio, 0.78; 95% confidence interval, 0.62-0.98). We identified a unique association between the rs6950857 genotype, seaweed intake, and MetS. These findings highlight the importance of VIPR2 and the regulatory role of seaweed consumption in MetS incidence.
Asunto(s)
Síndrome Metabólico , Algas Marinas , Masculino , Persona de Mediana Edad , Humanos , Síndrome Metabólico/epidemiología , Síndrome Metabólico/genética , Factores de Riesgo , Incidencia , Pueblos del Este de Asia , Verduras , República de Corea/epidemiología , Receptores de Tipo II del Péptido Intestinal VasoactivoRESUMEN
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.