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  1. NTU Theses and Dissertations Repository
  2. 公共衛生學院
  3. 流行病學與預防醫學研究所
請用此 Handle URI 來引用此文件: http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/89770
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dc.contributor.advisor林菀俞zh_TW
dc.contributor.advisorWan-Yu Linen
dc.contributor.author張學永zh_TW
dc.contributor.authorXue-Yong Changen
dc.date.accessioned2023-09-20T16:18:24Z-
dc.date.available2023-11-09-
dc.date.copyright2023-09-20-
dc.date.issued2023-
dc.date.submitted2023-06-27-
dc.identifier.citation1. Chang X-Y, Lin W-Y: Epigenetic age acceleration mediates the association between smoking and diabetes-related outcomes. Clinical Epigenetics 2023, 15(1):94.
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dc.identifier.urihttp://tdr.lib.ntu.edu.tw/jspui/handle/123456789/89770-
dc.description.abstract過去研究已發現吸菸會導致特定 DNA CpG 位點甲基化,進而增加對糖尿病的易感性和引發肺功能下降。本研究旨在探討由 DNA 甲基化生物標記造成的表觀遺傳年齡加速(EAA),是否在亞洲人種中與吸菸、糖尿病、肺功能之間存在中介效應。
本研究對於來自「臺灣人體生物資料庫」的 2,474 名參與者計算了五種不同的 EAA,包括 HannumEAA、IEAA、PhenoEAA、GrimEAA 和 DunedinPACE。結果顯示,GrimEAA、基於 DNA 甲基化的吸菸包年、DNA 甲基化中的第一型胞漿素原活化抑制劑 (PAI-1)、DunedinPACE 和 PhenoEAA 等標記會在吸菸與空腹血糖值和糖化血色素等糖尿病指標間有中介效應。另外,DNA 甲基化中的 PAI-1 也會中介吸菸與用力呼氣肺活量的關係,且戒菸長期來說會間接地透過 GrimEAA 正向影響用力呼氣肺活量。
研究結論表示,由 DNA 甲基化生物標記造成的表觀遺傳年齡加速,在吸菸與健康之間扮演著重要角色。總而言之,吸菸會直接或間接地透過與衰老相關的 DNA CpG 位點甲基化,損害人類健康,而 DNA 甲基化生物標記在此關係中存在中介效應。
zh_TW
dc.description.abstractSmoking has been found to cause changes in DNA methylation (DNAm) at specific cytosine-phosphate-guanine (CpG) sites, which can result in increased susceptibility to diabetes and decreased lung function. This study investigated the character of epigenetic age acceleration (EAA), caused by DNAm, in connecting the association between smoking and health outcomes related to diabetes and lung function within an Asian population.
Five distinct measurements of EAA were assessed in the study, including HannumEAA, IEAA, PhenoEAA, GrimEAA, and DunedinPACE, in 2,474 participants from the Taiwan Biobank. The results indicated that the associations between smoking and health outcomes related to diabetes, such as fasting glucose and hemoglobin A1c were mediated by several DNAm markers, namely GrimEAA, DNAm-based pack-years, DNAm plasminogen activator inhibitor 1 (PAI-1) levels, DunedinPACE, and PhenoEAA. Additionally, DNAm PAI-1 levels acted as a mediator in the relationship between smoking and forced vital capacity (FVC), a lung-related outcome. Furthermore, long-term smoking cessation had a beneficial impact on FVC among former smokers through the mediator GrimEAA.
The study’s findings highlight the effect of DNAm on EAA, establishing a crucial connection between smoking and health. It conclusively demonstrates that smoking directly impairs human health and indirectly affects it by inducing changes in DNAm CpG sites associated with aging. These changes in DNAm markers can mediate the complex relationship between smoking and health outcomes.
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dc.description.tableofcontentsSupporting Publication i
謝辭 ii
中文摘要 iii
Abstract iv
Contents vi
List of Figures vii
List of Tables viii
1. Introduction 1
2. Methods 11
2.1 Study Participants 11
2.2 Calculations of EAA (M) 12
2.3 Statistical Analysis 12
3. Results 18
3.1 Demographic Characteristics 18
3.2 Relationship Pathway from Exposure to Mediator (X → M) 21
3.3 Results of Mediation Analysis (X → M → Y) 26
4. Discussion 32
5. Conclusions 41
6. Figures 42
7. Tables 45
8. Reference 53
9. Supplementary 62
9.1 Additional analysis - SEM 62
9.2 Supplementary Figures 67
9.3 Supplementary Tables 77
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dc.language.isoen-
dc.subject肺功能zh_TW
dc.subject吸菸zh_TW
dc.subjectDNA甲基化zh_TW
dc.subject表觀遺傳年齡加速zh_TW
dc.subject糖尿病zh_TW
dc.subjectsmokingen
dc.subjectlung functionen
dc.subjectdiabetesen
dc.subjectepigenetic age accelerationen
dc.subjectDNA methylationen
dc.titleDNA甲基化生物標記對於吸菸、糖尿病、肺功能之中介效應zh_TW
dc.titleThe Mediation Effects of DNA Methylation on Smoking, Diabetes, and Lung Functionen
dc.typeThesis-
dc.date.schoolyear111-2-
dc.description.degree碩士-
dc.contributor.oralexamcommittee劉貞佑;馮嬿臻zh_TW
dc.contributor.oralexamcommitteeChen-Yu Liu ;Yen-Chen Fengen
dc.subject.keyword吸菸,DNA甲基化,表觀遺傳年齡加速,糖尿病,肺功能,zh_TW
dc.subject.keywordsmoking,DNA methylation,epigenetic age acceleration,diabetes,lung function,en
dc.relation.page87-
dc.identifier.doi10.6342/NTU202300910-
dc.rights.note未授權-
dc.date.accepted2023-06-28-
dc.contributor.author-college公共衛生學院-
dc.contributor.author-dept流行病學與預防醫學研究所-
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