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Zheng, Yan

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Zheng

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Yan

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Zheng, Yan
Author's Publications: search.filters.isAuthorOfPublication.cf2aa08d-ffa0-498b-844a-a00007db9b0b

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Now showing 1 - 7 of 7
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    Genome-wide association studies in East Asians identify new loci for waist-hip ratio and waist circumference
    (Nature Publishing Group, 2016) Wen, Wanqing; Kato, Norihiro; Hwang, Joo-Yeon; Guo, Xingyi; Tabara, Yasuharu; Li, Huaixing; Dorajoo, Rajkumar; Yang, Xiaobo; Tsai, Fuu-Jen; Li, Shengxu; Wu, Ying; Wu, Tangchun; Kim, Soriul; Guo, Xiuqing; Liang, Jun; Shungin, Dmitry; Adair, Linda S.; Akiyama, Koichi; Allison, Matthew; Cai, Qiuyin; Chang, Li-Ching; Chen, Chien-Hsiun; Chen, Yuan-Tsong; Cho, Yoon Shin; Choi, Bo Youl; Gao, Yutang; Go, Min Jin; Gu, Dongfeng; Han, Bok-Ghee; He, Meian; Hixson, James E.; Hu, Yanling; Huang, Tao; Isono, Masato; Jung, Keum Ji; Kang, Daehee; Kim, Young Jin; Kita, Yoshikuni; Lee, Juyoung; Lee, Nanette R.; Lee, Jeannette; Wang, Yiqin; Liu, Jian-Jun; Long, Jirong; Moon, Sanghoon; Nakamura, Yasuyuki; Nakatochi, Masahiro; Ohnaka, Keizo; Rao, Dabeeru; Shi, Jiajun; Sull, Jae Woong; Tan, Aihua; Ueshima, Hirotsugu; Wu, Chen; Xiang, Yong-Bing; Yamamoto, Ken; Yao, Jie; Ye, Xingwang; Yokota, Mitsuhiro; Zhang, Xiaomin; Zheng, Yan; Qi, Lu; Rotter, Jerome I.; Jee, Sun Ha; Lin, Dongxin; Mohlke, Karen L.; He, Jiang; Mo, Zengnan; Wu, Jer-Yuarn; Tai, E. Shyong; Lin, Xu; Miki, Tetsuro; Kim, Bong-Jo; Takeuchi, Fumihiko; Zheng, Wei; Shu, Xiao-Ou
    Sixty genetic loci associated with abdominal obesity, measured by waist circumference (WC) and waist-hip ratio (WHR), have been previously identified, primarily from studies conducted in European-ancestry populations. We conducted a meta-analysis of associations of abdominal obesity with approximately 2.5 million single nucleotide polymorphisms (SNPs) among 53,052 (for WC) and 48,312 (for WHR) individuals of Asian descent, and replicated 33 selected SNPs among 3,762 to 17,110 additional individuals. We identified four novel loci near the EFEMP1, ADAMTSL3 , CNPY2, and GNAS genes that were associated with WC after adjustment for body mass index (BMI); two loci near the NID2 and HLA-DRB5 genes associated with WHR after adjustment for BMI, and three loci near the CEP120, TSC22D2, and SLC22A2 genes associated with WC without adjustment for BMI. Functional enrichment analyses revealed enrichment of corticotropin-releasing hormone signaling, GNRH signaling, and/or CDK5 signaling pathways for those newly-identified loci. Our study provides additional insight on genetic contribution to abdominal obesity.
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    Habitual coffee consumption and genetic predisposition to obesity: gene-diet interaction analyses in three US prospective studies
    (BioMed Central, 2017) Wang, Tiange; Huang, Tao; Kang, Jae Hee; Zheng, Yan; Jensen, Majken; Wiggs, Janey; Pasquale, Louis; Fuchs, Charles; Campos, Hannia; Rimm, Eric; Willett, Walter; Hu, Frank; Qi, Lu
    Background: Whether habitual coffee consumption interacts with the genetic predisposition to obesity in relation to body mass index (BMI) and obesity is unknown. Methods: We analyzed the interactions between genetic predisposition and habitual coffee consumption in relation to BMI and obesity risk in 5116 men from the Health Professionals Follow-up Study (HPFS), in 9841 women from the Nurses’ Health Study (NHS), and in 5648 women from the Women’s Health Initiative (WHI). The genetic risk score was calculated based on 77 BMI-associated loci. Coffee consumption was examined prospectively in relation to BMI. Results: The genetic association with BMI was attenuated among participants with higher consumption of coffee than among those with lower consumption in the HPFS (P interaction = 0.023) and NHS (P interaction = 0.039); similar results were replicated in the WHI (P interaction = 0.044). In the combined data of all cohorts, differences in BMI per increment of 10-risk allele were 1.38 (standard error (SE), 0.28), 1.02 (SE, 0.10), and 0.95 (SE, 0.12) kg/m2 for coffee consumption of < 1, 1–3 and > 3 cup(s)/day, respectively (P interaction < 0.001). Such interaction was partly due to slightly higher BMI with higher coffee consumption among participants at lower genetic risk and slightly lower BMI with higher coffee consumption among those at higher genetic risk. Each increment of 10-risk allele was associated with 78% (95% confidence interval (CI), 59–99%), 48% (95% CI, 36–62%), and 43% (95% CI, 28–59%) increased risk for obesity across these subgroups of coffee consumption (P interaction = 0.008). From another perspective, differences in BMI per increment of 1 cup/day coffee consumption were 0.02 (SE, 0.09), –0.02 (SE, 0.04), and –0.14 (SE, 0.04) kg/m2 across tertiles of the genetic risk score. Conclusions: Higher coffee consumption might attenuate the genetic associations with BMI and obesity risk, and individuals with greater genetic predisposition to obesity appeared to have lower BMI associated with higher coffee consumption. Electronic supplementary material The online version of this article (doi:10.1186/s12916-017-0862-0) contains supplementary material, which is available to authorized users.
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    Metabolites of Glutamate Metabolism Are Associated With Incident Cardiovascular Events in the PREDIMED PREvención con DIeta MEDiterránea (PREDIMED) Trial
    (John Wiley and Sons Inc., 2016) Zheng, Yan; Hu, Frank; Ruiz‐Canela, Miguel; Clish, Clary B.; Dennis, Courtney; Salas‐Salvado, Jordi; Hruby, Adela; Liang, Liming; Toledo, Estefania; Corella, Dolores; Ros, Emilio; Fitó, Montserrat; Gómez‐Gracia, Enrique; Arós, Fernando; Fiol, Miquel; Lapetra, José; Serra‐Majem, Lluis; Estruch, Ramón; Martínez‐González, Miguel A.
    Background: Glutamate metabolism may play a role in the pathophysiology of cardiometabolic disorders. However, there is limited evidence of an association between glutamate‐related metabolites and, moreover, changes in these metabolites, and risk of cardiovascular disease (CVD). Methods and Results: Plasma levels of glutamate and glutamine were measured at baseline and 1‐year follow‐up in a case‐cohort study including 980 participants (mean age 68 years; 46% male) from the PREvención con DIeta MEDiterránea (PREDIMED) randomized trial, which assessed a Mediterranean diet intervention in the primary prevention of CVD. During median 4.8 years of follow‐up, there were 229 incident CVD events (nonfatal stroke, nonfatal myocardial infarction, or CVD death). In fully adjusted models, per 1‐SD, baseline glutamate was associated with 43% (95% CI: 16% to 76%) and 81% (39% to 137%) increased risk of composite CVD and stroke alone, respectively, and baseline glutamine‐to‐glutamate ratio with 25% (6% to 40%) and 44% (25% to 58%) decreased risk of composite CVD and stroke alone, respectively. Associations appeared linear for stroke (both P linear trend≤0.005). Among participants with high baseline glutamate, the interventions lowered CVD risk by 37% compared to the control diet; the intervention effects were not significant when baseline glutamate was low (P interaction=0.02). No significant effect of the intervention on year‐1 changes in metabolites was observed, and no effect of changes themselves on CVD risk was apparent. Conclusions: Baseline glutamate was associated with increased CVD risk, particularly stroke, and glutamine‐to‐glutamate ratio was associated with decreased risk. Participants with high glutamate levels may obtain greater benefits from the Mediterranean diet than those with low levels. Clinical Trial Registration URL: www.controlled-trials.com. Unique identifier: ISRCTN 35739639.
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    Genetic variation of fasting glucose and changes in glycemia in response to 2-year weight-loss diet intervention: the POUNDS Lost trial
    (2016) Wang, Tiange; Huang, Tao; Zheng, Yan; Rood, Jennifer; Bray, George A.; Sacks, Frank; Qi, Lu
    Objective: Weight loss intervention through diet modification has been widely used to improve obesity-related hyperglycemia; however, little is known about whether genetic variation modifies the intervention effect. We examined the interaction between weight-loss diets and genetic variation of fasting glucose on changes in glycemic traits in a dietary intervention trial. Research Design and Methods The Preventing Overweight Using Novel Dietary Strategies (POUNDS LOST) trial is a randomized, controlled 2-year weight-loss trial. We assessed overall genetic variation of fasting glucose by calculating a genetic risk score (GRS) based on 14 fasting glucose-associated single nucleotide polymorphisms, and examined the progression in fasting glucose and insulin levels, and insulin resistance and insulin sensitivity in 733 adults from this trial. Results: The GRS was associated with 6-month changes in fasting glucose (P<0.001), fasting insulin (P=0.042), homeostasis model assessment of insulin resistance (HOMA-IR, P=0.009) and insulin sensitivity (HOMA-S, P=0.043). We observed significant interaction between the GRS and dietary fat on 6-month changes in fasting glucose, HOMA-IR and HOMA-S after multivariable adjustment (P-interaction=0.007, 0.045, and 0.028, respectively). After further adjustment for weight loss, the interaction remained significant on change in fasting glucose (P=0.015). In the high-fat diet group, participants in the highest GRS tertile showed increased fasting glucose, whereas participants in the lowest tertile showed decreased fasting glucose (P-trend<0.001); in contrast, the genetic association was not significant in the low-fat diet group (P-trend=0.087). Conclusions: Our data suggest that participants with a higher genetic risk may benefit more by eating a low-fat diet to improve glucose metabolism.
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    DNA Methylation Variants at HIF3A Locus, B-Vitamin Intake, and Long-term Weight Change: Gene-Diet Interactions in Two U.S. Cohorts
    (American Diabetes Association, 2015) Huang, Tao; Zheng, Yan; Qi, Qibin; Xu, Min; Ley, Sylvia; Li, Yanping; Kang, Jae Hee; Wiggs, Janey; Pasquale, Louis; Chan, Andrew; Rimm, Eric; Hunter, David; Manson, JoAnn; Willett, Walter; Hu, Frank; Qi, Lu
    The first epigenome-wide association study of BMI identified DNA methylation at an HIF3A locus associated with BMI. We tested the hypothesis that DNA methylation variants are associated with BMI according to intake of B vitamins. In two large cohorts, we found significant interactions between the DNA methylation–associated HIF3A single nucleotide polymorphism (SNP) rs3826795 and intake of B vitamins on 10-year changes in BMI. The association between rs3826795 and BMI changes consistently increased across the tertiles of total vitamin B2 and B12 intake (all P for interaction <0.01). The differences in the BMI changes per increment of minor allele were −0.10 (SE 0.06), −0.01 (SE 0.06), and 0.12 (SE 0.07) within subgroups defined by increasing tertiles of total vitamin B2 intake and −0.10 (SE 0.06), −0.01 (SE 0.06), and 0.10 (SE 0.07) within subgroups defined by increasing tertiles of total vitamin B12 intake. In two independent cohorts, a DNA methylation variant in HIF3A was associated with BMI changes through interactions with total or supplemental vitamin B2, vitamin B12, and folate. These findings suggest a potential causal relation between DNA methylation and adiposity.
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    Folic Acid Supplementation and the Risk of Cardiovascular Diseases: A Meta‐Analysis of Randomized Controlled Trials
    (John Wiley and Sons Inc., 2016) Li, Yanping; Huang, Tianyi; Zheng, Yan; Muka, Tauland; Troup, Jenna; Hu, Frank
    Background: Results from observational and genetic epidemiological studies suggest that lower serum homocysteine levels are associated with lower incidence of cardiovascular disease (CVD). Numerous randomized controlled trials have investigated the efficacy of lowering homocysteine with folic acid supplementation for CVD risk, but conflicting results have been reported. Methods and Results: Three bibliographic databases (Medline, Embase, and the Cochrane Database of Systematic Reviews) were searched from database inception until December 1, 2015. Of the 1933 references reviewed for eligibility, 30 randomized controlled trials involving 82 334 participants were included in the final analysis. The pooled relative risks of folic acid supplementation compared with controls were 0.90 (95% CI 0.84–0.96; P=0.002) for stroke, 1.04 (95% CI 0.99–1.09; P=0.16) for coronary heart disease, and 0.96 (95% CI 0.92–0.99; P=0.02) for overall CVD. The intervention effects for both stroke and combined CVD were more pronounced among participants with lower plasma folate levels at baseline (both P<0.02 for interaction). In stratified analyses, a greater beneficial effect for overall CVD was seen in trials among participants without preexisting CVD (P=0.006 for interaction) or in trials with larger reduction in homocysteine levels (P=0.009 for interaction). Conclusions: Our meta‐analysis indicated a 10% lower risk of stroke and a 4% lower risk of overall CVD with folic acid supplementation. A greater benefit for CVD was observed among participants with lower plasma folate levels and without preexisting CVD and in studies with larger decreases in homocysteine levels. Folic acid supplementation had no significant effect on risk of coronary heart disease.
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    Circulating adiponectin and cardiovascular mortality in patients with type 2 diabetes mellitus: evidence of sexual dimorphism
    (BioMed Central, 2014) Menzaghi, Claudia; Xu, Min; Salvemini, Lucia; De Bonis, Concetta; Palladino, Giuseppe; Huang, Tao; Copetti, Massimiliano; Zheng, Yan; Li, Yanping; Fini, Grazia; Hu, Frank; Bacci, Simonetta; Qi, Lu; Trischitta, Vincenzo
    Background: The pathogenesis of cardiovascular (CV) mortality, whose rate is increased in type 2 diabetes, is poorly understood. While high serum adiponectin is associated with increased CV mortality in the general population, no data are available in type 2 diabetes. We here investigated whether this counterintuitive association was observable also in diabetic patients and whether it was sex-specific. Methods: Three prospective cohorts were analyzed: 1) Gargano Heart Study (GHS; 359 patients, 58 events/1,934 person-years; py); 2) Health Professional Follow-up Study (HPFS; 833 men, 146 events/10,024 py); 3) Nurses’ Health Study (NHS; 902 women, 144 events/15,074 py). Results: In GHS serum adiponectin predicted CV mortality in men (hazard ratio, HR, and 95% CI per standard deviation, SD, increment = 1.54, 1.19-2.01), but not women (HR = 0.98, 0.48-2.01). Circulating adiponectin predicted CV mortality in men from HPFS (HR = 1.44, 1.21-1.72), but not in women from NHS (HR = 1.08, 0.86-1.35), used as replication samples. In a pooled analysis, HRs were 1.47 (1.27-1.70) in 1,075 men and 1.07 (0.86-1.33) in 1,019 women (p for HRs heterogeneity across sexes = 0.018). Conclusions: This is the first report showing that high circulating adiponectin predicts increased CV mortality in men, but not in women with type 2 diabetes. Further studies are necessary to unravel the mechanisms through which adiponectin influences CV mortality in a sex-specific manner. Electronic supplementary material The online version of this article (doi:10.1186/s12933-014-0130-y) contains supplementary material, which is available to authorized users.