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| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 潘敏雄(Min-Hsiung Pan) | |
| dc.contributor.author | Hai-Ching Pung | en |
| dc.contributor.author | 馮采晴 | zh_TW |
| dc.date.accessioned | 2021-06-17T08:09:52Z | - |
| dc.date.available | 2026-03-08 | |
| dc.date.copyright | 2021-04-07 | |
| dc.date.issued | 2021 | |
| dc.date.submitted | 2021-03-11 | |
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| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/73771 | - |
| dc.description.abstract | 在高脂飲食中，不僅僅是導致全身性低度發炎反應亦代謝性內毒素血症 (metabolic endotoxemia)，影響腸道菌群組成進而可能加劇肥胖之形成。近期研究表示，硫化多醣 (Sulphated polysaccharide) 可通過改善腸道菌群，減少代謝異常並維持腸道上皮細胞的完整性來預防高脂飲食誘導的肥胖。然而，青絲藻中 (Ulva prolifera) 的硫化多醣對於延緩肥胖和代謝疾病的機制仍尚未有更進一步的研究。因此，本研究將製備青絲藻多醣並針對高脂飲食誘導小鼠所造成之脂質蓄積、代謝異常及腸道菌群變化進行深入的探討。小鼠飼養期間將利用管餵的方式介入青絲藻多醣 (100，300，500 mg/kg) 並持續15周。結果顯示，青絲藻多醣具延緩小鼠肥胖和改善代謝異常的效果，其中包括粥狀動脈硬化指標 (atherogenic index) 的下降，顯示青絲藻多醣有降低高脂飲食所誘導的心血管疾病發生。蘇木精-伊紅染色結果發現，青絲藻多醣減緩肝臟中脂肪浸潤和脂肪細胞肥大之情形。另外，分別在小鼠的血液、肝臟及脂肪組織中所測得的細胞激素濃度也有下降的趨勢，顯示經由青絲藻多醣的介入後可減少全身性低度發炎反應。從西方墨點法的結果發現，青絲藻多醣可能通過增加脂聯素活性並提高了AMPK的表現量。 有趣的是，由於CPT-1和PPAR 表現量同时升高，青絲藻多醣可能透過PPAR 激动剂增强了-氧化，以達到減脂的效果。 此外，青絲藻多醣也改善了肥胖小鼠中的腸道菌群，其中發現經由青絲藻多醣介入後增加Parasutterella、Feacalibaculum 和 Bifidobacterium，同時減少了Acetatifactor、 Tyzerella、 Ruminococcus 1和Desulfovibrio的豐富度，而菌群的變化可能具有改善肥胖和代謝異常的效果。綜合上述，青絲藻多醣可以減緩高脂飲食誘導的小鼠肥胖及相關代謝疾病之效果，且可能可以營造出一個更健康的腸道環境並有利於益生菌的生長。 | zh_TW |
| dc.description.abstract | Obesity is characterized by low-grade inflammation and accompanying an altered and less diverse gut microbiota composition during a fat-enriched diet. Recently studies indicate that sulphated polysaccharide prevents high-fat diet induced obesity, reduces metabolic disorder, and restores the gut microbiota. However, Ulva prolifera polysaccharide may induce anti-obesogenic effects that have not been examined. Therefore, the present study investigates the possibility of UPP extraction that may prevent diet-induced obesity and metabolic disorder and modulating gut microbiota composition. High-fat diet (HFD)-fed mice are treated with UPP (100, 300, 500mg/kg) by intragastric gavage for 15 weeks. The effects of polysaccharide will be assessed by western blot to determine the lipid metabolism pathway and 16S rDNA-based microbiota analysis to identify the gut bacteria enriched by UPP. The results showed that UPP considerably slowed down the HFD-induced weight gain and improved metabolic disorders in HFD-fed mice. Notably, the effects were associated with reduced adipose tissue hypertrophy, triglyceride concentration in liver and systemic low-grade inflammation, and improved fasting blood glucose. Moreover, our result reveals that UPP may elevate the expression of AMPK via adiponectin activation . Interestingly, we found that UPP may induce PPAR-alpha agonist to enhance beta-oxidation since the elevation of CPT-1 and PPAR-alpha expression simultaneously. Meanwhile, gut microbiota analysis revealed UPP promoted the growth of Parasutterella, Feacalibaculum, and Bifidobacterium, and reduced the abundance of Acetatifactor, Tyzerella, Ruminococcus_1, and Desulfovibrio. The changes in microbiota may have a positively correlated effect on improving obesity and metabolic abnormalities. In summary, UPP may prevent the effects of HFD-induced obesity and the associated metabolic diseases, and may modulate the composition of gut microbiota to facilitate the growth of probiotic. | en |
| dc.description.provenance | Made available in DSpace on 2021-06-17T08:09:52Z (GMT). No. of bitstreams: 1 U0001-0803202115351900.pdf: 16630651 bytes, checksum: 0730ed9089e8a2933a6454694554736f (MD5) Previous issue date: 2021 | en |
| dc.description.tableofcontents | 口試委員會審定書 I 謝誌 II 摘要 IV Abstract VI Table of content VIII Appendix XI List of figures XII List of tables XIV Abbreviations XV 1. Literature Review 1 1.1 Obesity 1 I. Definition 1 II. Obesity causes and consequence 2 III. Prevention and treatment 3 1.2 Adipose tissue 4 I. Function of adipose tissue 4 II. Introduction of adipokines 5 1.3 Regulation of adipocytes 7 I. Adipogenesis 7 II. Lipogenesis 9 III. Lipolysis 10 IV. β-oxidation 12 1.4 Marine algae 13 I. Introduction of marine algae 13 II. Biological activities of marine green macroalgae 14 III. Ulva prolifera and polysaccharide 15 2. Objective and Experimental Design 16 3. Materials and Methods 18 3.1 Material 18 I. Equipment and Instruments 18 II. Chemicals and Reagent 19 III. Sample 20 3.2 Method 20 I. Ulva prolifera Polysaccharide Preparation 20 II. Animal and Treatment Protocol 21 III. Animal Sacrification 22 IV. Hematoxylin Eosin stain (H E stain) 23 V. Protein Extraction 26 VI. Protein Quantitation Assays 27 VII. Western Blotting 29 VIII. Fasting Blood Glucose Test 33 IX. Oral Glucose Tolerance Test (OGTT) 34 X. Colonic Microbiota Analysis 35 XI. Measurement of Cytokine 36 4. Result and Discussion 40 4.1 Monosaccharide composition of Ulva prolifera 40 4.2 Effects of UPPs on body weight in HFD-fed C57BL/6 mice 40 4.3 Effects of UPPs on daily intake and food efficiency ratio in HFD-fed C57BL/6 mice 42 4.4 Effects of UPPs on visceral fat pad weight and visceral adiposity index in HFD-fed C57BL/6 mice 43 4.5 Effects of UPPs on organ weight and appearance in HFD-fed C57BL/6 mice 44 4.6 Effects of UPPs on liver tissue and amount of TG in HFD-fed C57BL/6 mice 45 4.7 Effects of UPPs on serum biochemical parameter in HFD-fed C57BL/6 mice 46 4.8 Effects of UPPs on fasting blood glucose and glucose tolerance in HFD-fed C57BL/6 mice 47 4.9 Effects of UPPs on cytokine in HFD-fed C57BL/6 mice 48 4.10 Effects of UPPs on adiponectin expression in HFD-fed C57BL/6 mice 49 4.11 Effects of UPPs on p-AMPK/AMPK expression in HFD-fed C57BL/6 mice 50 4.12 Effects of UPPs on adipogenesis in HFD-fed C57BL/6 mice 50 4.13 Effects of UPPs on lipogenesis in HFD-fed C57BL/6 mice 51 4.14 Effects of UPPs on lipolysis in HFD-fed C57BL/6 mice 52 4.15 Effects of UPPs on β-oxidation in HFD-fed C57BL/6 mice 53 4.16 Effects of UPPs on short-chain fatty acid in HFD-fed C57BL/6 mice 54 4.17 Effects of UPPs on intestinal microbiota composition in HFD-fed C57BL/6 mice 55 5. Conclusion 57 6. Figure and Table 58 7. Reference 82 | |
| dc.language.iso | en | |
| dc.subject | 肥胖 | zh_TW |
| dc.subject | 硫化多醣 | zh_TW |
| dc.subject | 青絲藻 | zh_TW |
| dc.subject | 腸道菌相 | zh_TW |
| dc.subject | 代謝紊亂 | zh_TW |
| dc.subject | gut microbiota | en |
| dc.subject | metabolic disorder | en |
| dc.subject | Obesity | en |
| dc.subject | sulphated polysaccharide | en |
| dc.subject | Ulva prolifera | en |
| dc.title | 青絲藻多醣透過調升脂聯素與調節腸道菌相抑制高脂飲食誘導小鼠肥胖之功效 | zh_TW |
| dc.title | Ulva prolifera polysaccharide exerts anti-obesity effect via up-regulation of adiponectin expression and gut microbiota modulation in high-fat diet fed C57BL/6 mice | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 109-2 | |
| dc.description.degree | 碩士 | |
| dc.contributor.oralexamcommittee | 羅翊禎(Yi-Chen Lo),黃步敏(Bu-Miin Huang),郭靜娟(Ching-Chuan Kuo),何元順(Yuan-Soon Ho) | |
| dc.subject.keyword | 肥胖,代謝紊亂,腸道菌相,青絲藻,硫化多醣, | zh_TW |
| dc.subject.keyword | Obesity,metabolic disorder,gut microbiota,Ulva prolifera,sulphated polysaccharide, | en |
| dc.relation.page | 87 | |
| dc.identifier.doi | 10.6342/NTU202100779 | |
| dc.rights.note | 有償授權 | |
| dc.date.accepted | 2021-03-12 | |
| dc.contributor.author-college | 生物資源暨農學院 | zh_TW |
| dc.contributor.author-dept | 食品科技研究所 | zh_TW |
| 顯示於系所單位： | 食品科技研究所 | |
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