Recent genetic association studies have identified 55 genetic loci associated with obesity or body mass index (BMI). The vast majority, 51 loci, however, were identified in European-ancestry populations. We conducted a meta-analysis of associations between BMI and ∼2.5 million genotyped or imputed single nucleotide polymorphisms among 86 757 individuals of Asian ancestry, followed by in silico and de novo replication among 7488-47 352 additional Asian-ancestry individuals. We identified four novel BMI-associated loci near the KCNQ1 (rs2237892, P = 9.29 × 10(-13)), ALDH2/MYL2 (rs671, P = 3.40 × 10(-11); rs12229654, P = 4.56 × 10(-9)), ITIH4 (rs2535633, P = 1.77 × 10(-10)) and NT5C2 (rs11191580, P = 3.83 × 10(-8)) genes. The association of BMI with rs2237892, rs671 and rs12229654 was significantly stronger among men than among women. Of the 51 BMI-associated loci initially identified in European-ancestry populations, we confirmed eight loci at the genome-wide significance level (P < 5.0 × 10(-8)) and an additional 14 at P < 1.0 × 10(-3) with the same direction of effect as reported previously. Findings from this analysis expand our knowledge of the genetic basis of obesity.

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The aim of this study was to describe the incidence of metabolic syndrome and to identify five components as metabolic syndrome predictors. The final study included 1,095 subjects enrolled in a rural part of Daegu Metropolitan City, Korea for a cohort study in 2003. Of these, 762 (69.6%) subjects had participated in the repeat survey. During the five-year follow-up, incidence density was significantly higher for women than for men (men, 30.0/1,000 person-years; women, 46.4/1,000 person-years). In both men and women, incidence of metabolic syndrome showed a significant increase with increasing number of metabolic syndrome components at baseline. Compared with individuals presenting none of components at baseline, relative risks were increased 1.22 (men; 95% CI, 0.43-3.51), 2.21 (women; 95% CI, 0.98-4.97) times more for individuals with one component of metabolic syndrome and 5.30 (men; 95% CI, 2.31-12.13), 5.53 (women; 95% CI, 2.78-11.01) times more for those who had two components. In multivariate analysis, the most powerful risk factor for metabolic syndrome was abdominal obesity in men and low HDL-cholesterol in women (adjusted relative risk, 3.28, 2.53, respectively). Consequently, finding a high risk group for metabolic syndrome according to gender and prevention of metabolic syndrome through lifestyle modification are essential.

The relationship between dietary Zn intake and the risk of atherosclerosis remains unclear, and no epidemiological studies have been reported on the effects of dietary Zn intake on morphological changes in the vascular wall. We examined the relationship between dietary Zn intake and common carotid intima-media thickness (IMT) as a marker of subclinical atherosclerosis among the middle-aged and elderly populations. A cross-sectional analysis of a prospective cohort baseline study was performed with 4564 adults aged 40–89 years and free of clinical CVD. Dietary data were collected by trained interviewers using an FFQ. Common carotid IMT was measured using a B-mode ultrasound imaging technique. Subclinical atherosclerosis was determined using carotid IMT, and defined as >80th percentile of carotid IMT or ≥ 1 mm of carotid IMT. After adjustment for potential confounders, the mean carotid IMT in the low Zn intake group was higher than that in the high Zn intake group. When subclinical atherosclerosis was defined as >80th percentile value of IMT or ≥ 1 mm of carotid IMT, after adjustment for potential confounders, Zn intake was inversely related to subclinical atherosclerosis (5thv.1st quintile, OR 0·64, 95 % CI 0·45, 0·90,Pfor trend = 0·069; 5thv.1st quintile, OR 0·34, 95 % CI 0·16, 0·70,Pfor trend = 0·005, respectively). In persons free of clinical CVD, dietary Zn intake was inversely correlated with subclinical atherosclerosis. The present findings suggest a putative protective role of dietary Zn intake against the development of atherosclerosis.