臺灣博碩士論文加值系統

本研究主要探討幾丁聚醣降低 streptozotocin-nicotinamide 所誘發耐糖不良大白鼠其脂肪組織之影響。以雄性 Sprague-Dawley 大白鼠為實驗動物，利用皮下注射 nicotinamide (230 mg/kg BW) 及 streptozotocin (65 mg/kg BW) 誘發產生耐糖不良之症狀。實驗共分為四組，分別是 (1) 控制組 (Normal control) (2) 耐糖不良組 (IGT) (3) 5% 幾丁聚醣組 (IGT+5% CS) (4) 7% 幾丁聚醣組 (IGT+7% CS)，實驗共進行十週，飼養期間大白鼠採自由飲食。實驗結果顯示，攝取幾丁聚醣明顯抑制耐糖不良大白鼠體重、肝臟重量及脂肪組織重量 (腎周圍脂肪+副睪脂肪)，其中以 7% 幾丁聚醣效果最為顯著。在血漿生化值方面，攝取 5%、7% 幾丁聚醣都具有降低耐糖不良大白鼠血漿葡萄糖、HOMA-IR 值、總膽固醇、TNF-α、IL-6、瘦體素、維生素 E 濃度、AST 和ALT 活性並提升血漿脂泌素、類昇醣素胜肽濃度。此外，研究中亦發現攝取幾丁聚醣會顯著提升耐糖不良大白鼠血漿、肝臟脂質過氧化物濃度及血漿三酸甘油酯、游離脂肪酸濃度。在肝臟脂質方面，攝取 5%、7% 幾丁聚醣都能降低耐糖不良大白鼠肝臟脂質堆積。另外，脂肪組織變化方面，攝取幾丁聚醣皆能有效抑制脂肪細胞增大、副睪脂肪細胞三酸甘油酯堆積，而攝取 7% 幾丁聚醣能顯著提高糖尿病大白鼠腎周圍脂肪、副睪組織 LPL 活性及脂解作用速率並減少副睪脂肪細胞 TG 含量。此外，攝取 5%、7% 幾丁聚醣均能顯著提升肝臟 PPARαmRNA 基因及副睪脂肪 UCP1 的表現量。綜合以上結果，推測幾丁聚醣可能藉由提升體內 PPARα基因表現，調控下游 UCP1 蛋白質表現增加其產熱效應，提升脂肪組織脂解速率，而達到調節脂質代謝之功效。

壹、前言 1
貳、文獻整理 3
一、幾丁質和幾丁聚醣的簡介 3
1. 幾丁質之來源與分佈 3
2. 幾丁質與幾丁聚醣的結構 3
3. 幾丁質與幾丁聚醣的特性與應用 5
二、糖尿病 8
1. 糖尿病簡介 8
2. 糖尿病的診斷及分類 8
3. 糖尿病對醣類代謝及脂質代謝之影響 12
三、糖尿病研究之動物模式 13
1. 研究糖尿病的動物模式 13
2. Streptozotocin (STZ) 與Nicotinamide化學誘導糖尿病的動物模式 14
四、過氧化體增殖劑活化受器 (peroxisome proliferator activated receptors, PPARs) 19
1. 過氧化體 19
2. 過氧化體增殖劑 20
3. PPARs 的緣起 20
4. PPARs 的種類與分佈 21
5. PPARs 的結構與功能 22
6. PPARs 的作用模式 23
7. PPARs 的生理效應 23
五、脂肪組織與胰島素阻抗之相關性 26
六、脂肪細胞分解脂質之調控- lipolysis 作用 30
七、Uncoupling proteins (UCPs) 家族之介紹 32
八、幾丁聚醣對於脂質代謝之影響 34
參、實驗動機與目的 37
肆、實驗設計 38
一、實驗流程 38
二、實驗材料 39
1. 實驗動物 39
2. 實驗飼料 40
3. 幾丁聚醣 40
4. 實驗儀器 40
三、實驗方法 42
1. 幾丁聚醣去乙醯度、黏度及平均分子量之測定 42
2. 動物分組 44
3. 動物飼養及樣品收集 45
4. 樣品分析 45
伍、結果 63
陸、討論 69
柒、結論 88
捌、參考文獻 89

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