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| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 沈立言 | zh_TW |
| dc.contributor.advisor | Lee-Yan Sheen | en |
| dc.contributor.author | 陳冰倩 | zh_TW |
| dc.contributor.author | Bing-Qian Chen | en |
| dc.date.accessioned | 2025-07-23T16:27:14Z | - |
| dc.date.available | 2025-07-24 | - |
| dc.date.copyright | 2025-07-23 | - |
| dc.date.issued | 2025 | - |
| dc.date.submitted | 2025-07-07 | - |
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| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/98012 | - |
| dc.description.abstract | 心血管疾病（Cardiovascular disease, CVD）是全球主要死亡原因之一。日益增多的證據表明，腸道菌叢在調節心血管疾病相關風險因子（包括高血壓、高血糖、高血脂、慢性發炎及動脈粥狀硬化）中扮演著至關重要的角色。由腸道微生物衍生的代謝物，如短鏈脂肪酸（Short-chain fatty acids, SCFA）和氧化三甲胺（Trimethylamine N-oxide, TMAO），與調控CVD的進程及嚴重程度有關。近期研究發現，源自苯丙胺酸（Phenylalanine, PHE）微生物代謝的苯乙酰谷氨酰胺（Phenylacetylglutamine, PAGln）及其小鼠類似物苯乙酰甘胺酸（Phenylacetylglycine, PAGly），與心血管疾病的死亡率增加有關。這些影響被認為是透過增強腎上腺素受體的訊息傳遞，進而促進血栓形成和導致心臟衰竭。然而，先前的研究僅採用腹腔注射給藥，以誘導體內PAGln/PAGly短暫升高，此方式可能無法準確反映生理條件下，這些代謝物經由未消化完的苯丙胺酸緩慢發酵生成的真實情況。為了能更貼近生物體的變化以模擬慢性暴露的影響，本研究透過飲用水給予小鼠PAGln/PAGly，並結合AAV-mPCSK9誘導的動脈粥狀硬化模型，探討其對肥胖、高膽固醇血症及動脈粥狀硬化的作用。實驗將小鼠分為四組，分別餵食添加控制組（水）、PAGln、PAGly或PHE的西方飲食（Western diet, WD），持續12週。實驗過程中發現，長期攝取PAGln/PAGly可顯著降低小鼠的體重、肥胖程度、胰島素阻抗及肝臟發炎。此效果可能是透過活化棕色脂肪組織中的β3-腎上腺素受體，以及其所依賴的解偶聯蛋白-1（Uncoupling protein 1, Ucp-1）介導的粒線體產熱作用所達成。另一方面，PAGln/PAGly的暴露亦會導致心率和血壓升高，這可能歸因於其具有類似腎上腺素的活性。值得注意的是，儘管給予PAGln的小鼠膽固醇水平受到控制，其動脈粥狀硬化斑塊的形成卻更為顯著。本研究首次揭示了PAGln/PAGly在心臟代謝疾病中所扮演的多面向角色，突顯其同時作為保護因子與致病因子的雙重特性，而這可能源於複雜的腎上腺素受體訊息傳遞。鑑於其在心血管疾病中作為「雙面刃」微生物代謝物的潛力，未來有必要進行更深入的機制探討，特別是針對腎上腺素受體所介導的各種表型，例如心臟衰竭、免疫調節及粒線體功能。 | zh_TW |
| dc.description.abstract | Cardiovascular disease (CVD) remains one of the leading causes of death globally. Increasing evidence suggests that the gut microbiota plays a crucial role in modulating CVD-related risk factors, including hypertension, hyperglycemia, hyperlipidemia, chronic inflammation, and atherosclerosis. Gut microbiota-derived metabolites such as short-chain fatty acids (SCFAs) and trimethylamine N-oxide (TMAO) have been implicated in modulating the progression and severity of CVD. Recently, phenylacetylglutamine (PAGln) and its murine analog, phenylacetylglycine (PAGly)—both derived from the microbial metabolism of phenylalanine (PHE)—have been linked to increased cardiovascular mortality. These effects are thought to be mediated by enhanced thrombosis and heart failure via adrenergic receptor signaling. However, previous studies utilized only intraperitoneal (i.p.) administration to induce transiently high systemic levels of PAGln/PAGly. This approach may not accurately reflect physiological conditions, where these metabolites are produced slowly through the microbial fermentation of undigested phenylalanine. To better simulate chronic exposure, we administered PAGln/PAGly to mice via their drinking water and applied an AAV-mPCSK9-induced atherosclerosis model to investigate their impact on obesity, hypercholesterolemia, and atherosclerosis. Mice were assigned to four groups and fed a Western diet (WD) supplemented with either water, PAGln, PAGly, or PHE for 12 weeks.
Interestingly, chronic exposure to PAGln/PAGly significantly reduced body weight, adiposity, insulin resistance, and liver inflammation, likely through the activation of β3-adrenergic receptors and subsequent Ucp-1-dependent mitochondrial thermogenesis in brown adipose tissue. Conversely, PAGln/PAGly exposure also increased heart rate and blood pressure, presumably due to their norepinephrine-like adrenergic activity. Notably, while their cholesterol levels were controlled, PAGln-treated mice developed more pronounced atherosclerotic plaque formation. This study is the first to reveal the multifaceted roles of PAGln/PAGly in cardiometabolic diseases, underscoring their dual function as both protective and pathogenic agents, a duality likely arising from complex adrenergic receptor signaling. Given their potential as double-edged microbial metabolites in CVD, further mechanistic studies are warranted, particularly those focusing on adrenergic receptor-mediated phenotypes such as heart failure, immune modulation, and mitochondrial function. | en |
| dc.description.provenance | Submitted by admin ntu (admin@lib.ntu.edu.tw) on 2025-07-23T16:27:14Z No. of bitstreams: 0 | en |
| dc.description.provenance | Made available in DSpace on 2025-07-23T16:27:14Z (GMT). No. of bitstreams: 0 | en |
| dc.description.tableofcontents | 目 次
口試委員會審定書 I 謝辭 II 中文摘要 III 英文摘要 IV 目 次 VI 圖目次 IX 表目次 XI 縮寫表 XII 第一章 文獻回顧 1 第一節 心血管疾病 1 一、 心血管疾病定義及流行病學 1 二、 心血管疾病危險因子 2 第二節 動脈粥狀硬化 4 一、 動脈粥狀硬化疾病進程 4 二、 動脈粥狀硬化致病機轉 4 三、 動脈粥狀硬化之動物誘導模式 6 四、 ssAAV8/hAAT-mPCSK9 7 五、 粥狀動脈硬化治療 7 第三節 腸道菌與動脈粥狀硬化的關聯性 9 一、 腸道菌在人體扮演的角色 9 二、 腸道菌與心血管疾病之聯繫 9 三、 飲食、腸道菌與心血管疾病之因果關係 11 第四節 苯丙氨酸之代謝物-PAGln/PAGly 14 一、 PAGln/PAGly之生成 14 二、 調控PAA產生之關鍵基因 15 三、 PAGln與心血管疾病之關係 16 四、 PAGln/PAGly 對代謝系統潛在影響之推論 17 第二章 研究假說與實驗架構 18 第一節 研究假說 18 第二節 實驗架構 19 第三章 實驗材料與方法 20 第一節 材料與儀器設備 20 一、 實驗儀器及設備 20 二、實驗藥品 21 第二節 實驗方法 24 一、 PAGln劑量設計及製備 24 二、 動物實驗 24 三、 血漿生化值分析 26 四、 肝臟及脂肪組織病理學分析 27 五、 心臟冷凍切片 28 六、 油紅染色 28 七、 小鼠血壓分析 29 八、 即時聚合酶連鎖反應(Quantitative real time PCR, RT-PCR) 29 第三節 統計分析 30 第四章 結果 31 第一節 小鼠血清標靶代謝體分析 31 第二節 小鼠體重變化分析 31 第三節 小鼠液體攝取量變化分析 31 第四節 小鼠血糖變化分析 32 第五節 小鼠血清生化參數評估 32 第六節 小鼠肝臟病變分析 32 第七節 小鼠臟器變化分析 33 第八節 小鼠脂肪組織病變分析 33 第九節 小鼠棕色脂肪相關產熱基因分析 34 第十節 小鼠血壓與心率分析 34 第十一節 小鼠主動脈斑塊之定量分析 35 第十二節 小鼠主動脈弓黏附因子分析 35 第五章 討論 36 第一節 小鼠血漿標靶代謝體分析 36 第二節 介入PAGln/PAGly/PHE後小鼠的血糖穩態改善效果 37 第三節 介入PAGln/PAGly/PHE後小鼠的肝臟病變程度討論 39 第四節 小鼠棕色脂肪的相關產熱基因分析 40 第五節 小鼠血壓脈搏分析 41 第六節 小鼠主動脈斑塊的嚴重程度 42 第七節 小鼠主動脈弓黏附因子分析 43 第六章 結論 45 第七章 圖表 47 第八章 參考文獻 63 Manuscript 80 References 115 | - |
| dc.language.iso | zh_TW | - |
| dc.subject | 腸道菌叢 | zh_TW |
| dc.subject | 粒線體 | zh_TW |
| dc.subject | 腎上腺素受體 | zh_TW |
| dc.subject | 動脈粥狀硬化 | zh_TW |
| dc.subject | 心血管疾病 | zh_TW |
| dc.subject | PAGln | zh_TW |
| dc.subject | Atherosclerosis | en |
| dc.subject | Cardiovascular disease | en |
| dc.subject | Gut microbiota | en |
| dc.subject | PAGln | en |
| dc.subject | Mitochondria | en |
| dc.subject | Adrenergic receptor | en |
| dc.title | 探討腸道菌代謝物苯乙酰基谷氨酸與苯乙酰基甘胺酸在心血管疾病發展過程中所扮演的角色 | zh_TW |
| dc.title | Investigating the Role of Gut Microbial Metabolites Phenylacetylglutamine and Phenylacetylglycine in Cardiovascular Disease | en |
| dc.type | Thesis | - |
| dc.date.schoolyear | 113-2 | - |
| dc.description.degree | 碩士 | - |
| dc.contributor.oralexamcommittee | 吳明賢;郭錦樺;吳偉愷 | zh_TW |
| dc.contributor.oralexamcommittee | Ming-Shiang Wu;Ching-Hua Kuo;Wei-Kai Wu | en |
| dc.subject.keyword | PAGln,腸道菌叢,心血管疾病,動脈粥狀硬化,腎上腺素受體,粒線體, | zh_TW |
| dc.subject.keyword | PAGln,Gut microbiota,Cardiovascular disease,Atherosclerosis,Adrenergic receptor,Mitochondria, | en |
| dc.relation.page | 117 | - |
| dc.identifier.doi | 10.6342/NTU202501573 | - |
| dc.rights.note | 同意授權(限校園內公開) | - |
| dc.date.accepted | 2025-07-09 | - |
| dc.contributor.author-college | 生物資源暨農學院 | - |
| dc.contributor.author-dept | 食品科技研究所 | - |
| dc.date.embargo-lift | 2030-07-06 | - |
| 顯示於系所單位： | 食品科技研究所 | |
文件中的檔案：
| 檔案 | 大小 | 格式 | |
|---|---|---|---|
| ntu-113-2.pdf 未授權公開取用 | 4.17 MB | Adobe PDF | 檢視/開啟 |
系統中的文件，除了特別指名其著作權條款之外，均受到著作權保護，並且保留所有的權利。