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Mechanism of Glycitein in the Treatment of Colon Cancer Based on Network Pharmacology and Molecular Docking. 基于网络药理学和分子对接的甘菊素治疗结肠癌的机制
IF 2.6 4区 医学 Q3 GENETICS & HEREDITY Pub Date : 2023-01-01 Epub Date: 2022-09-30 DOI: 10.1159/000527124
Tao Xiang, Weibiao Jin

Introduction: The prevalence of colon cancer remains high across the world. The early diagnosis of colon cancer is challenging. Moreover, patients with colon cancer frequently suffer from poor prognoses.

Methods: Differentially expressed genes (DEGs) in colon cancer were acquired based on TCGA-COAD dataset screening. DEGs were input into the Connectivity Map (CMap) database to screen small molecule compounds with the potential to reverse colon cancer pathological function. Glycitein ranked first among the screened small-molecule compounds. We downloaded the main targets of glycitein from the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP) database and constructed protein-protein interaction (PPI) networks of those which were closely related to targets by the Search Tool for the Retrieval of Interaction Gene/Proteins (STRING). Five potential targets of glycitein for treating colon cancer were identified (CCNA2, ESR1, ESR2, MAPK14, and PTGS2). These targets were used as seeds for random walk with restart (RWR) analysis of PPI networks. Then, the interaction network of glycitein-colon cancer-related genes was constructed based on the top 50 genes in affinity coefficients. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were conducted on the potential genes targeted by glycitein in colon cancer treatment and those that were closely bound up with targets.

Results: GO analysis demonstrated that the enrichment of these genes was primarily discovered in biological functions including regulation of fibroblast proliferation, response to oxygen levels, and epithelial cell proliferation. The KEGG analysis results illustrated that the signaling pathways where these genes were mostly involved consisted of the mitogen-activated protein kinase signaling pathway, the phosphatidylinositol-3-kinase-Akt signaling pathway, and the p53 signaling pathway. Finally, stable binding of glycitein to five potential targets in colon cancer was verified by molecular docking.

Conclusion: This study elucidated the key targets and main pathways of glycitein on the basis of network pharmacology and preliminarily analyzed molecular mechanisms in the treatment of colon cancer. A scientific basis is provided for glycitein application in treating colon cancer.

介绍:结肠癌在全球的发病率居高不下。结肠癌的早期诊断具有挑战性。此外,结肠癌患者的预后往往很差:方法:根据 TCGA-COAD 数据集筛选获得结肠癌中的差异表达基因(DEGs)。将 DEGs 输入连接图(CMap)数据库,筛选出有可能逆转结肠癌病理功能的小分子化合物。在筛选出的小分子化合物中,甘氨肽排名第一。我们从中药系统药理学数据库和分析平台(TCMSP)中下载了甘桔素的主要靶点,并利用检索相互作用基因/蛋白的搜索工具(STRING)构建了与靶点密切相关的蛋白-蛋白相互作用(PPI)网络。确定了甘草亭治疗结肠癌的五个潜在靶点(CCNA2、ESR1、ESR2、MAPK14 和 PTGS2)。这些靶点被用作种子,用于 PPI 网络的随机行走与重启(RWR)分析。然后,根据亲和系数排名前 50 位的基因构建了甘氨酸-结肠癌相关基因的相互作用网络。对甘氨酸在结肠癌治疗中的潜在靶向基因以及与靶点紧密结合的基因进行了基因本体(GO)和京都基因组百科全书(KEGG)富集分析:GO分析表明,这些基因的富集主要体现在成纤维细胞增殖调控、对氧水平的反应和上皮细胞增殖等生物学功能方面。KEGG分析结果表明,这些基因主要参与的信号通路包括丝裂原活化蛋白激酶信号通路、磷脂酰肌醇-3-激酶-Akt信号通路和p53信号通路。最后,通过分子对接验证了甘草亭与结肠癌五个潜在靶点的稳定结合:本研究在网络药理学的基础上阐明了甘草亭的关键靶点和主要通路,初步分析了甘草亭治疗结肠癌的分子机制。为甘草亭在结肠癌治疗中的应用提供了科学依据。
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引用次数: 0
Abstracts - 16th Congress of the International Society of Nutrigenetics & Nutrigenomics. 摘要-国际营养遗传学和营养基因组学学会第16届大会。
IF 2.6 4区 医学 Q3 GENETICS & HEREDITY Pub Date : 2023-01-01 Epub Date: 2023-10-05 DOI: 10.1159/000534171
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引用次数: 0
Impact of Methyl-Donor Micronutrient Supplementation on DNA Methylation Patterns: A Systematic Review and Meta-Analysis of in vitro, Animal, and Human Studies. 甲基供体微量营养素补充对DNA甲基化模式的影响:体外、动物和人类研究的系统综述和荟萃分析。
IF 2.6 4区 医学 Q3 GENETICS & HEREDITY Pub Date : 2023-01-01 Epub Date: 2023-11-07 DOI: 10.1159/000533193
Jhulia Caroline N L da Mota, Amanda A Ribeiro, Lucas M Carvalho, Gabriel P Esteves, Sofia M Sieczkowska, Karla F Goessler, Bruno Gualano, Carolina F Nicoletti

Background: DNA methylation patterns are directly associated with diverse metabolic disorders. The status of methyl-donor micronutrients has been associated with DNA methylation levels, and altered ingestion of folate, choline, betaine, B vitamins and methionine may impact genes both globally and at the level of promoter regions. Despite this, the role of methyl-donor micronutrient supplementation on DNA methylation profiles is currently unclear.

Objectives: The aims of this systematic review and meta-analysis were to identify and synthesize the evidence about methyl-donor nutrient supplementation on DNA methylation.

Methods: A systematic literature search was performed in Medline, Embase, Scopus, and Web of Science databases with a combination of terms related to DNA methylation assessment, supplementation, and methyl-donor nutrients. Studies (in vitro, animal models, or human clinical trials) were included if DNA methylation levels after any kind of methyl-donor micronutrient supplementation or treatment was investigated. Studies were assessed for bias using Revised Cochrane risk-of-bias tool for randomized trials, risk-of-bias in Non-randomized Studies of Interventions or Systematic Review Centre for Laboratory Animal Experimentation tools. Data were extracted from studies measuring DNA methylation levels in any sample or tissue, following any kind of methyl-donor micronutrient supplementation or treatment. Separate random-effects meta-analyses were performed for animal model studies and human clinical trials that examined the effects of folic acid supplementation on DNA methylation.

Results: Fifty-seven studies were included in this systematic review: 18 human clinical trials, 35 in animal model, and 4 in vitro studies. Concerning overall risk of bias, most of the studies were classified as "high risk" or "some concerns." Meta-analysis with meta-regression from studies in animal models showed that folic acid dose significantly affected DNA methylation and that high and very high doses showed increases in DNA methylation when compared to low doses. However, meta-analysis of human clinical trials showed that folic acid supplementation did not promote significant changes in DNA methylation when compared to placebo.

Conclusion: Folic acid supplementation may change global DNA methylation levels in animals supplemented with high, as compared to low, doses. Heterogeneity in studies and supplementation protocols make it difficult to establish clinical recommendations. However, these effects, even if small, might be of clinical importance in the management of patients with diseases related to DNA hypomethylation.

背景:DNA甲基化模式与多种代谢紊乱直接相关。甲基供体微量营养素的状况与DNA甲基化水平有关,叶酸、胆碱、甜菜碱、B族维生素和甲硫氨酸的摄入改变可能会在全球和启动子区域水平上影响基因。尽管如此,甲基供体微量营养素补充对DNA甲基化特征的作用目前尚不清楚。目的:本系统综述和荟萃分析的目的是识别和综合甲基供体营养素补充对DNA甲基化的影响。方法:在MEDLINE、EMBASE、SCOPUS和Web of Sciences数据库中进行系统的文献检索,结合与DNA甲基化评估、补充和甲基供体营养素相关的术语。如果研究了任何类型的甲基供体微量营养素补充或治疗后的DNA甲基化水平,则包括研究(体外、动物模型或人类临床试验)。使用随机试验的改良Cochrane偏倚风险工具、非随机干预研究中的偏倚风险或实验室动物实验系统审查中心工具评估研究的偏倚。数据是从测量任何样本或组织中DNA甲基化水平的研究中提取的,在任何类型的甲基供体微量营养素补充或治疗后。分别对动物模型研究和人体临床试验进行了随机效应荟萃分析,研究了补充叶酸对DNA甲基化的影响。结果:57项研究被纳入系统综述:18项人体临床试验,35项动物模型研究和4项体外研究。关于偏倚的总体风险,大多数研究被归类为“高风险”或“一些担忧”。动物模型研究的荟萃分析和荟萃回归显示,叶酸剂量显著影响DNA甲基化,与低剂量相比,高剂量和极高剂量显示DNA甲基化增加。然而,来自人类临床试验的荟萃分析表明,与安慰剂相比,补充叶酸不会促进DNA甲基化的显著变化。结论:与低剂量相比,高剂量补充叶酸可能会改变动物的整体DNA甲基化水平。研究和补充方案的异质性使得制定临床建议变得困难。然而,这些影响,即使很小,也可能对DNA低甲基化相关疾病患者的管理具有临床重要性。
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引用次数: 0
Exploring the Associations and Molecular Impacts of miR-146a/rs2910164 and miR-196a2/rs185070757 with Rheumatoid Arthritis in a Pakistani Population. 在巴基斯坦人群中探讨miR-146a/rs2910164和miR-196a/rs185070757与类风湿性关节炎的相关性和分子影响。
IF 2.6 4区 医学 Q3 GENETICS & HEREDITY Pub Date : 2023-01-01 Epub Date: 2023-06-27 DOI: 10.1159/000526937
Yasir Ali, Aamir Khan, Mehran Akhtar, Suleman Khan, Zia Ul Islam, Nadia Farooqi, Aftab Ali Shah, Yangchao Chen, Fazal Jalil

Introduction: MicroRNAs (miRNAs) are a new class of molecules that participate in post-transcriptional regulation of gene expression and hence have been reported to have a crucial role in the pathogenesis of rheumatoid arthritis (RA). We aimed to investigate the association of miR-146a rs2910164 (G/C) and miR-196a2 rs185070757 (T/G) with RA susceptibility in Pakistani patients and to bioinformatically predict the molecular function of these miRNAs.

Methods: A case-control study on 600 individuals was conducted, including 300 RA patients and 300 matching healthy controls. Genotyping was performed by tetra-primer amplification of refractory mutation system-polymerase chain reaction, and the association between variants and RA was statistically determined using different models.

Results: For the variant rs2910164 (G/C) in miR-146a, no difference in genotype distribution was observed between RA cases and controls, as determined using co-dominant (χ2 = 4.33; p = 0.114), homozygous dominant (C/C vs. G/G + C/G) (OR = 0.740 [0.531-1.032]; p = 0.091), homozygous recessive (G/G vs. C/C + G/C) (odds ratio [OR] = 01.432 [0.930-2.206]; p = 0.126), heterozygous (G/C vs. C/C + G/G) (OR = 1.084 [0.786-1.494]; p = 0.682), and additive (OR 0.778 [0.617-0.981]; p = 0.039) models. Similarly, the GT genotype in the rs185070757 (T/G) miR-196a2 variant did not differ between cases and controls with any models (p > 0.05). For the first time, we report no association of miR-146a rs2910164 (G/C) and miR-196a2 rs185070757 (T/G) with RA in a Pakistani population. A subsequent bioinformatic analysis revealed that the CC genotype of miR-146a rs2910164 might have a protective role against RA pathogenesis, with no effect observed with the miR-196a2 rs185070757.

Conclusion: Our findings suggest that these miRNAs might have little-to-no impact on the RA pathogenesis in the Pakistani population.

引言:微小RNA(miRNA)是一类参与基因表达转录后调控的新分子,因此已被报道在类风湿性关节炎(RA)的发病机制中发挥着至关重要的作用。我们旨在研究miR-146a rs2910164(G/C)和miR-196a2 rs185070757(T/G)与巴基斯坦患者RA易感性的关系,并从生物信息学角度预测这些miRNA的分子功能。通过难治性突变系统聚合酶链式反应的四引物扩增进行基因分型,并使用不同的模型统计确定变异与RA之间的关联。结果:对于miR-146a中的变异体rs2910164(G/C),RA病例和对照组之间没有观察到基因型分布的差异,这是通过共显性(χ2=4.33;p=0.114)、纯合显性(C/C vs.G/G+C/G)(OR=0.740[0.531-1.032];p=0.091)、纯合子隐性(G/G vs.C/C+G/C)(比值比[OR]=0.1432[0.930-2.26];p=0.126)、杂合(G/C vs。C/C+G/G)(OR=1.084[0.76-1494];p=0.682)和加性(OR0.778[0.617-0.981];p=0.039)模型。同样,rs185070757(T/G)miR-196a2变体中的GT基因型在病例和任何模型的对照组之间都没有差异(p>0.05)。我们首次报道了在巴基斯坦人群中miR-146a rs2910164(G/C)和miR-196a2rs185070755(T/G)与RA没有关联。随后的生物信息学分析显示,miR-146a rs2910164的CC基因型可能对RA的发病机制具有保护作用,而miR-196a2 rs185070757没有观察到影响。结论:我们的研究结果表明,这些miRNA可能对巴基斯坦人群的RA发病机制几乎没有影响。
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引用次数: 0
Abdominal Obesity, Excessive Adiposity, and the Taq1B CETP Variant Are Positively Associated with Serum Lipid Levels in Mexican Women. 墨西哥妇女的腹部肥胖、过度肥胖和 Taq1B CETP 变异与血清脂质水平呈正相关。
IF 2.6 4区 医学 Q3 GENETICS & HEREDITY Pub Date : 2023-01-01 Epub Date: 2023-01-18 DOI: 10.1159/000529053
Mariana Perez-Robles, Wendy Campos-Perez, Joel Torres-Vanegas, Sarai Citlalic Rodriguez-Reyes, Juan José Rivera-Valdés, Erika Martínez-Lopez

Introduction: Obesity is a prevalent multifactorial disease whose main complication is dyslipidemia. Serum lipid levels also depend on genetic factors including the Taq1B variant of the CETP gene, which is suggested to be influenced by environmental factors and adiposity. Therefore, this study aimed to determine the effect of the Taq1B CETP variant on serum lipid levels associated with anthropometrical variables.

Methods: 165 women from western Mexico were enrolled in this cross-sectional study. Weight and body fat were measured by bioimpedance and waist circumference with a measuring tape. Serum lipid levels were determined by dry chemistry. The Taq1B CETP variant was analyzed by allelic discrimination.

Results: Women with abdominal obesity and the B1B2/B2B2 genotype had significantly higher total cholesterol levels (195.17 [185.95-204.39] vs. 183 mg/dL [169.83-196.16], p = 0.007) and low density lipoprotein (118.84 [110.65-127.03] vs. 113.84 mg/dL [102.37-125.31], p = 0.037) than carriers of the B1B1 genotype. Likewise, subjects with excessive adiposity and the B1B2/B2B2 genotype showed significantly higher total cholesterol levels (195.05 [186.04-204.06] vs. 182.40 mg/dL [169.03-195.76], p = 0.003) than those with the B1B1 genotype.

Conclusion: Women with abdominal obesity or excessive adiposity, who are also carriers of the B1B2/B2B2 genotype, have higher serum lipid levels than women with the B1B1 genotype.

引言肥胖症是一种普遍存在的多因素疾病,其主要并发症是血脂异常。血清脂质水平也取决于遗传因素,包括 CETP 基因的 Taq1B 变体。因此,本研究旨在确定 Taq1B CETP 变体对血清脂质水平的影响与人体测量变量的关系。体重和体脂用生物阻抗测量,腰围用卷尺测量。血清脂质水平通过干化学法测定。通过等位基因辨别分析了 Taq1B CETP 变体:结果:腹部肥胖和 B1B2/B2B2 基因型女性的总胆固醇水平(195.17 [185.95-204.39] vs. 183 mg/dL [169.83-196.16],p = 0.007)和低密度脂蛋白水平(118.84 [110.65-127.03] vs. 113.84 mg/dL [102.37-125.31],p = 0.037)明显高于 B1B1 基因型携带者。同样,过度肥胖和 B1B2/B2B2 基因型受试者的总胆固醇水平(195.05 [186.04-204.06] vs. 182.40 mg/dL [169.03-195.76],p = 0.003)也明显高于 B1B1 基因型受试者:结论:腹部肥胖或过度肥胖的女性,如果也是 B1B2/B2B2 基因型携带者,其血清脂质水平要高于 B1B1 基因型女性。
{"title":"Abdominal Obesity, Excessive Adiposity, and the Taq1B CETP Variant Are Positively Associated with Serum Lipid Levels in Mexican Women.","authors":"Mariana Perez-Robles, Wendy Campos-Perez, Joel Torres-Vanegas, Sarai Citlalic Rodriguez-Reyes, Juan José Rivera-Valdés, Erika Martínez-Lopez","doi":"10.1159/000529053","DOIUrl":"10.1159/000529053","url":null,"abstract":"<p><strong>Introduction: </strong>Obesity is a prevalent multifactorial disease whose main complication is dyslipidemia. Serum lipid levels also depend on genetic factors including the Taq1B variant of the CETP gene, which is suggested to be influenced by environmental factors and adiposity. Therefore, this study aimed to determine the effect of the Taq1B CETP variant on serum lipid levels associated with anthropometrical variables.</p><p><strong>Methods: </strong>165 women from western Mexico were enrolled in this cross-sectional study. Weight and body fat were measured by bioimpedance and waist circumference with a measuring tape. Serum lipid levels were determined by dry chemistry. The Taq1B CETP variant was analyzed by allelic discrimination.</p><p><strong>Results: </strong>Women with abdominal obesity and the B1B2/B2B2 genotype had significantly higher total cholesterol levels (195.17 [185.95-204.39] vs. 183 mg/dL [169.83-196.16], p = 0.007) and low density lipoprotein (118.84 [110.65-127.03] vs. 113.84 mg/dL [102.37-125.31], p = 0.037) than carriers of the B1B1 genotype. Likewise, subjects with excessive adiposity and the B1B2/B2B2 genotype showed significantly higher total cholesterol levels (195.05 [186.04-204.06] vs. 182.40 mg/dL [169.03-195.76], p = 0.003) than those with the B1B1 genotype.</p><p><strong>Conclusion: </strong>Women with abdominal obesity or excessive adiposity, who are also carriers of the B1B2/B2B2 genotype, have higher serum lipid levels than women with the B1B1 genotype.</p>","PeriodicalId":18030,"journal":{"name":"Lifestyle Genomics","volume":" ","pages":"83-89"},"PeriodicalIF":2.6,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9094840","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
A Nutrigenetic Approach to Investigate ApoB EcoR1 Polymorphism–Dietary Acid Load Interactions on Lipid and Anthropometric-Related Outcomes in Adults with Dyslipidemic Type 2 Diabetes 研究ApoB-EcoR1多态性的营养遗传学方法——饮食酸负荷相互作用对2型糖尿病成人血脂异常和人体测量相关结果的影响
IF 2.6 4区 医学 Q3 GENETICS & HEREDITY Pub Date : 2022-12-14 DOI: 10.1159/000528656
Zeinab Naeini, Faezeh Abaj, Z. Esmaeily, E. Alvandi, Masoumeh Rafiee, F. Koohdani
Introduction: Despite multiple studies which have considered the role of dietary acid load (DAL) or Apolipoprotein B (ApoB) EcoR1 polymorphism in diabetes, none have assessed their interplay effect on metabolic markers. Therefore, this study aimed to determine the interaction of EcoR1 and DAL on metabolic markers among adults with Type 2 diabetes mellitus (T2DM).Methods: 492 randomly selected individuals with T2DM were recruited for this cross-sectional study. Dietary intake was evaluated by a validated food frequency questionnaire. DAL was assessed as net-endogenous acid production (NEAP) and potential renal acid load (PRAL). Real-time-PCR was used to genotype EcoR1. Metabolic markers were also assessed. The interaction effect of the polymorphism and DAL indexes was analyzed by analysis of covariance (ANCOVA). Result: The frequency of EcoR1 genotypes was not different between dyslipidemic and normolipidemic participants (P>0.05). Among participants with dyslipidemia, those with the GG genotype and who consumed a higher level of NEAP had higher body mass index (BMI) (p=0.03) and waist circumference (WC; p =0.02). Moreover, triglyceride (TG) concentration (P=0.007), the LDL/HDL ratio (P=0.03) and the TG/HDL (P=0.03) ratio were significantly higher in A allele carriers with higher than the median intake of NEAP, in comparison with GG homozygotes. Finally, GA/AA carriers who had a higher intake of PRAL had a higher TG concentration (P=0.006) and TG/HDL ratio (P=0.01) compared to lower median intake in the dyslipidemia group. Discussion/Conclusion: In the dyslipidemic group, there was a higher TG concentration among individuals with the GA/AA genotype and a higher intake of NEAP/ PRAL. Also, in this group, a higher intake of NEAP may be considered as a risk factor for increased levels of BMI and WC among participants with the GG genotype.
引言:尽管多项研究考虑了饮食酸负荷(DAL)或载脂蛋白B(ApoB)EcoR1多态性在糖尿病中的作用,但没有一项研究评估它们对代谢标志物的相互作用。因此,本研究旨在确定EcoR1和DAL对成人2型糖尿病(T2DM)代谢标志物的相互作用。方法:随机选择492名T2DM患者进行横断面研究。饮食摄入量通过一份经过验证的食物频率问卷进行评估。DAL评估为内源性净产酸量(NEAP)和潜在肾脏酸负荷(PRAL)。采用实时PCR技术对EcoR1进行基因分型。还评估了代谢标志物。通过协方差分析(ANCOVA)分析多态性与DAL指标的交互作用。结果:血脂异常和血脂正常参与者的EcoR1基因型频率没有差异(P>0.05)。在血脂异常参与者中,GG基因型和NEAP水平较高的参与者具有较高的体重指数(BMI)(P=0.03)和腰围(WC;P=0.02)。此外,甘油三酯(TG)浓度(P=0.007),NEAP摄入量高于中位数的A等位基因携带者的LDL/HDL比率(P=0.03)和TG/HDL比率(P=0.003)显著高于GG纯合子。最后,与血脂异常组的中位摄入量较低相比,PRAL摄入量较高的GA/AA携带者具有较高的TG浓度(P=0.006)和TG/HDL比率(P=0.01)。讨论/结论:在血脂异常组中,GA/AA基因型个体的TG浓度较高,NEAP/PRAL摄入量较高。此外,在这一组中,较高的NEAP摄入量可能被认为是GG基因型参与者BMI和WC水平升高的风险因素。
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引用次数: 1
Understanding Gene-Lifestyle Interaction in Obesity: The Role of Mediation versus Moderation 了解基因-生活方式在肥胖中的相互作用:调解与调节的作用
IF 2.6 4区 医学 Q3 GENETICS & HEREDITY Pub Date : 2022-03-01 DOI: 10.1159/000523813
L. Pérusse, Raphaëlle Jacob, V. Drapeau, C. Llewellyn, B. Arsenault, A. Bureau, M. Labonté, A. Tremblay, M. Vohl
Background: Obesity results from complex interactions between genetic susceptibility to weight gain and poor eating and lifestyle behaviors. The approach that has been traditionally used in genetics to investigate gene-environment/lifestyle interaction in obesity is based on the concept of moderation or effect modification. Another approach called mediation analysis can be used to investigate gene-environment interaction in obesity. The objective of this review article is to explain the differences between the concepts of moderation and mediation and summarize the studies that have used mediation analysis to support the role of eating or lifestyle behaviors as putative mediators of genetic susceptibility to obesity. Summary: Moderation is used to determine whether the effect of an exposure (genes associated with obesity) on an outcome (obesity phenotype) differs in magnitude and/or direction across the spectrum of environmental exposure. Mediation analysis is used to assess the extent to which the effect of the exposure on the outcome is explained by a given set of hypothesized mediators with the aim of understanding how the exposure could lead to the outcome. In comparison with moderation, relatively few studies used mediation analyses to investigate gene-environment interaction in obesity. Most studies found evidence that traits related to appetite or eating behaviors partly mediated genetic susceptibility to obesity in either children or adults. Key Messages: Moderation and mediation represent two complementary approaches to investigate gene-environment interaction in obesity and address different research questions pertaining to the cause-effect relationship between genetic susceptibility to obesity and various obesity outcomes. More studies relying on mediation are needed to better understand the role of eating and lifestyle habits in mediating genetic susceptibility to obesity.
背景:肥胖是体重增加的遗传易感性与不良饮食和生活方式行为之间复杂的相互作用的结果。传统上用于遗传学研究肥胖中基因-环境/生活方式相互作用的方法是基于适度或影响改变的概念。另一种称为中介分析的方法可用于研究肥胖的基因-环境相互作用。这篇综述文章的目的是解释适度和中介概念之间的差异,并总结使用中介分析来支持饮食或生活方式行为作为假定的肥胖遗传易感性中介作用的研究。摘要:适度用于确定暴露(与肥胖相关的基因)对结果(肥胖表型)的影响在不同的环境暴露范围内是否在大小和/或方向上有所不同。中介分析用于评估暴露对结果的影响在多大程度上可以通过一组假设的中介来解释,目的是了解暴露如何导致结果。与适度相比,相对较少的研究使用中介分析来调查肥胖的基因-环境相互作用。大多数研究发现,与食欲或饮食行为相关的特征在一定程度上介导了儿童或成人肥胖的遗传易感性。关键信息:调节和中介是研究肥胖中基因-环境相互作用的两种互补方法,并解决有关肥胖遗传易感性与各种肥胖结局之间因果关系的不同研究问题。为了更好地理解饮食和生活习惯在调节肥胖遗传易感性方面的作用,还需要更多依赖中介的研究。
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引用次数: 5
Dairy Product Intake Modifies MicroRNA Expression among Individuals with Hyperinsulinemia: A Post-Intervention Cross-Sectional Study 乳制品摄入改变高胰岛素血症患者MicroRNA表达:干预后横断面研究
IF 2.6 4区 医学 Q3 GENETICS & HEREDITY Pub Date : 2022-02-25 DOI: 10.1159/000523809
Leila Khorraminezhad, I. Rudkowska
Introduction: MicroRNA (miRNA) profiles have been shown to change after intake of dairy products. Dysregulation of miRNA is associated with the changes in the level of glycemic parameters. The objectives are: (1) to investigate miRNA expression after consumption of dairy products and (2) to study the association between miRNAs and glycemic profile among individuals with hyperinsulinemia. Methods: In crossover design, 24 participants were randomized into 2 phases: high dairy (HD) (≥4 servings/day according to the Canadian food guide [2007]) and adequate dairy (AD) (≤2 servings/day) over 6 weeks. First, miRNAs were extracted from a pooled plasma sample of 10 subjects after HD and AD intervention which analyzed in duplicate by array hybridization (Affymetrix Gene Chip miRNA Array v. 4.0). Second, 6 miRNAs related to type 2 diabetes (T2D) were validated by quantitative reverse transcription polymerase chain reaction (qRT-PCR) from plasma of 24 participants. Results: Microarray analysis indicated that 297 miRNAs expressed differentially (FC ≥ ±1.2; p value <0.05) in a pooled plasma sample of 10 subjects. Among pooled miRNAs, the level of selected miRNAs, including miR-652-3p, miR-106b-5p, miR-93-5p, and miR-107 were downregulated; conversely, miR-223-3p and miR-122-5p were upregulated. After qRT-PCR validation, only the expression level of miR-106-5p tended to be increased after HD compared to AD (p = 0.06). After AD intervention, the level of fasting plasma glucose (FPG) and insulin and homeostatic model assessment of insulin resistance were negatively correlated with miR-122-5p. Similarly, negative correlation was found between miR-106-5p and FPG. Conclusion: The miRNAs profile was modified after HD compared to AD, and this may have role in modifying the risk of T2D (registration No. NCT02961179).
引言:摄入乳制品后,微小核糖核酸(miRNA)谱发生了变化。miRNA的失调与血糖参数水平的变化有关。目的是:(1)研究食用乳制品后miRNA的表达;(2)研究高胰岛素血症患者的miRNA与血糖水平之间的关系。方法:在交叉设计中,24名参与者被随机分为两个阶段:高乳制品(HD)(根据加拿大食品指南[2007],每天≥4份)和充足乳制品(AD)(≤2份/天),为期6周。首先,从HD和AD干预后的10名受试者的合并血浆样本中提取miRNA,并通过阵列杂交(Affymetrix Gene Chip miRNA array v.4.0)进行重复分析。其次,通过定量逆转录聚合酶链反应(qRT-PCR)从24名参与者的血浆中验证了6种与2型糖尿病(T2D)相关的miRNA。结果:微阵列分析表明,在10名受试者的合并血浆样本中,297个miRNA差异表达(FC≥±1.2;p值<0.05)。在合并的miRNA中,所选miRNA的水平下调,包括miR-652-3p、miR-106b-5p、miR-93-5p和miR-107;相反,miR-223-3p和miR-122-5p被上调。qRT-PCR验证后,与AD相比,HD后只有miR-106-5p的表达水平倾向于增加(p=0.06)。AD干预后,空腹血糖(FPG)和胰岛素水平以及胰岛素抵抗的稳态模型评估与miR-122-5p呈负相关。同样,miR-106-5p与FPG之间也存在负相关。结论:与AD相比,HD后的miRNAs谱发生了改变,这可能在改变T2D的风险中发挥作用(注册号NCT02961179)。
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引用次数: 4
The rs9939609 Variant in FTO Increases the Risk of Hypercholesterolemia in Metabolically Healthy Subjects with Excess Weight. FTO中的rs9939609变异增加了超重代谢健康受试者高胆固醇血症的风险
IF 2.6 4区 医学 Q3 GENETICS & HEREDITY Pub Date : 2022-01-01 DOI: 10.1159/000527097
Erika Sierra-Ruelas, Wendy Campos-Pérez, Nathaly Torres-Castillo, Pablo García-Solís, Barbara Vizmanos, Erika Martínez-López

Introduction: The fat mass and obesity-associated gene (FTO) is largely/primarily expressed in the hypothalamus. It plays a role in energy balance, regulation of food intake, and adipogenesis. According to metabolic phenotypes, studies have associated the FTO rs9939609 variant with body mass index (BMI), body fat mass, and dietary intake but not with serum lipids. This study aimed to analyze the association of the FTO rs9939609 variant with serum lipids in Mexican adults with different metabolic phenotypes.

Methods: We included 306 subjects aged 18-65 years, classified as normal weight or excess weight (EW) according to their BMI. EW included BMI from 25 to 39.9 kg/m2. Participants were classified into two metabolic phenotypes: metabolically healthy/metabolically unhealthy (MH/MUH). We use the homeostatic model assessment of insulin resistance and NCEP-ATP III cutoffs for glucose, triglycerides, high-density lipoprotein, and blood pressure. Subjects with ≥2 altered parameters were classified as MUH. The variant was determined by allelic discrimination with TaqMan® probes.

Results: In subjects with the A allele, significantly higher total cholesterol and low-density-lipoprotein cholesterol were found (p < 0.05). Furthermore, subjects with EW-MH and the AA or AT genotype had a significantly higher odds ratio for hypercholesterolemia (odds ratio 4.48, 95% confidence interval: 1.48-13.59, p = 0.008).

Conclusion: The FTO rs9939609 variant may influence serum lipid concentrations, increasing the risk of hypercholesterolemia.

脂肪量和肥胖相关基因(FTO)主要在下丘脑表达。它在能量平衡、调节食物摄入和脂肪形成中起作用。根据代谢表型,研究发现FTO rs9939609变异与体重指数(BMI)、体脂量和饮食摄入有关,但与血脂无关。本研究旨在分析具有不同代谢表型的墨西哥成年人FTO rs9939609变异与血脂的关系。方法:306例年龄在18-65岁之间,根据体重指数分为正常体重和超重体重(EW)。EW包括BMI从25到39.9 kg/m2。参与者被分为两种代谢表型:代谢健康/代谢不健康(MH/MUH)。我们使用稳态模型评估胰岛素抵抗和NCEP-ATP III切断葡萄糖、甘油三酯、高密度脂蛋白和血压。参数改变≥2项的受试者被归类为MUH。用TaqMan®探针进行等位基因鉴定。结果:携带A等位基因的受试者总胆固醇和低密度脂蛋白胆固醇显著升高(p < 0.05)。此外,EW-MH和AA或AT基因型的受试者发生高胆固醇血症的比值比显著更高(比值比4.48,95%可信区间:1.48-13.59,p = 0.008)。结论:FTO rs9939609变异可能影响血脂浓度,增加高胆固醇血症的发生风险。
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引用次数: 0
Influences of the Interactions of Genetic Variations of Seven Core Circadian Clock Genes with Lifestyle Factors on Metabolic Parameters. 7个核心生物钟基因遗传变异与生活方式因素相互作用对代谢参数的影响
IF 2.6 4区 医学 Q3 GENETICS & HEREDITY Pub Date : 2022-01-01 DOI: 10.1159/000525859
Kimiko Yamakawa-Kobayashi, Sayaka Ishikawa, Nagi Miyake, Yuya Ohhara, Toshinao Goda

Introduction: In mammals, circadian rhythms regulate many behavioral and physiological processes. Genetic and epidemiological studies have shown that dysregulation of the circadian rhythm induces chronic metabolic diseases, such as obesity, diabetes, and dyslipidemia. We aimed to know the interactions of genetic variations of seven core circadian clock genes with lifestyle factors on the determination of metabolic parameters.

Methods: We have analyzed the impacts of genotype of seven core circadian clock genes (i.e., CLOCK, BMAL1, PER1, PER2, PER3, CRY1, and CRY2) and lifestyle factors (i.e., physical activity and sleep duration) in 575 Japanese males on the determination of metabolic parameters (i.e., body mass index [BMI], serum glucose, glycated hemoglobin [HbA1c], low-density lipoprotein cholesterol [LDL-C], and high-density lipoprotein cholesterol [HDL-C] levels).

Results: We have detected the associations between genotypes of PER3 and serum HbA1c level and genotypes of CRY1 and serum LDL-C level. Additionally, the interactions of the genotypes of PER1 and PER3 with physical activity for determining BMI, the genotypes of CLOCK with physical activity for determining serum HbA1c levels were observed. Furthermore, for determining serum HDL-C levels, the interactions of the genotypes of CRY2 with physical activity or sleep duration were observed.

Discussion/conclusion: Our findings indicate that the interactions of genotypes for core circadian clock genes and lifestyle factors (i.e., physical activity and sleep duration) are important for determining metabolic parameters.

在哺乳动物中,昼夜节律调节着许多行为和生理过程。遗传学和流行病学研究表明,昼夜节律失调可诱发慢性代谢性疾病,如肥胖、糖尿病和血脂异常。我们的目的是了解七个核心生物钟基因的遗传变异与生活方式因素对代谢参数决定的相互作用。方法:我们分析了575名日本男性7个核心生物钟基因(clock、BMAL1、PER1、PER2、PER3、CRY1和CRY2)的基因型和生活方式因素(即体力活动和睡眠时间)对代谢参数(即体重指数[BMI]、血清葡萄糖、糖化血红蛋白[HbA1c]、低密度脂蛋白胆固醇[LDL-C]和高密度脂蛋白胆固醇[HDL-C]水平)测定的影响。结果:我们检测到了PER3基因型与血清HbA1c水平、CRY1基因型与血清LDL-C水平的相关性。此外,我们还观察了PER1和PER3基因型与体力活动测定BMI的相互作用,以及CLOCK基因型与体力活动测定血清HbA1c水平的相互作用。此外,为了确定血清HDL-C水平,观察了CRY2基因型与身体活动或睡眠时间的相互作用。讨论/结论:我们的研究结果表明,核心生物钟基因的基因型与生活方式因素(即体力活动和睡眠时间)的相互作用对于确定代谢参数很重要。
{"title":"Influences of the Interactions of Genetic Variations of Seven Core Circadian Clock Genes with Lifestyle Factors on Metabolic Parameters.","authors":"Kimiko Yamakawa-Kobayashi,&nbsp;Sayaka Ishikawa,&nbsp;Nagi Miyake,&nbsp;Yuya Ohhara,&nbsp;Toshinao Goda","doi":"10.1159/000525859","DOIUrl":"https://doi.org/10.1159/000525859","url":null,"abstract":"<p><strong>Introduction: </strong>In mammals, circadian rhythms regulate many behavioral and physiological processes. Genetic and epidemiological studies have shown that dysregulation of the circadian rhythm induces chronic metabolic diseases, such as obesity, diabetes, and dyslipidemia. We aimed to know the interactions of genetic variations of seven core circadian clock genes with lifestyle factors on the determination of metabolic parameters.</p><p><strong>Methods: </strong>We have analyzed the impacts of genotype of seven core circadian clock genes (i.e., CLOCK, BMAL1, PER1, PER2, PER3, CRY1, and CRY2) and lifestyle factors (i.e., physical activity and sleep duration) in 575 Japanese males on the determination of metabolic parameters (i.e., body mass index [BMI], serum glucose, glycated hemoglobin [HbA1c], low-density lipoprotein cholesterol [LDL-C], and high-density lipoprotein cholesterol [HDL-C] levels).</p><p><strong>Results: </strong>We have detected the associations between genotypes of PER3 and serum HbA1c level and genotypes of CRY1 and serum LDL-C level. Additionally, the interactions of the genotypes of PER1 and PER3 with physical activity for determining BMI, the genotypes of CLOCK with physical activity for determining serum HbA1c levels were observed. Furthermore, for determining serum HDL-C levels, the interactions of the genotypes of CRY2 with physical activity or sleep duration were observed.</p><p><strong>Discussion/conclusion: </strong>Our findings indicate that the interactions of genotypes for core circadian clock genes and lifestyle factors (i.e., physical activity and sleep duration) are important for determining metabolic parameters.</p>","PeriodicalId":18030,"journal":{"name":"Lifestyle Genomics","volume":"15 4","pages":"124-130"},"PeriodicalIF":2.6,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10453189","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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Lifestyle Genomics
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