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研究生:陳宗德
研究生(外文):ChungDe Chen
論文名稱:Prednisolone改變飲食誘導肥胖小鼠體內鉻元素之分布
論文名稱(外文):Prednisolone Altered Chromium Distribution in Diet-Induced Obesity Mice
指導教授:毛嘉洪
指導教授(外文):Frank Chiahung Mao
學位類別:碩士
校院名稱:國立中興大學
系所名稱:獸醫學系
學門:獸醫學門
學類:獸醫學類
論文種類:學術論文
論文出版年:2005
畢業學年度:93
語文別:中文
論文頁數:99
中文關鍵詞:鉻元素糖尿病鉻元素肥胖症類固醇
外文關鍵詞:ChromiumDiabetes mellitusObesityPrednisolone
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肥胖症是造成胰島素阻抗、第2型糖尿病、心血管疾病的主要危險因子,現已清楚瞭解,肥胖症會促使形成代謝症候群與第2型糖尿病。臨床醫學在人類與動物試驗長期使用類固醇,會導致代謝症候群症狀如肥胖、胰島素阻抗、葡萄糖耐受性不良及高血糖症。現今,鉻元素已被證實為一個胰島素作用之輔助因子,可協助細胞內運送葡萄糖之代謝,增進細胞胰島素敏感性作用,進而改善體內血糖濃度,以預防糖尿病。在動物實驗與人體試驗指出,補充鉻元素可有效改善因類固醇糖尿病所引起之症狀。Clodfelder等人在2004年發現,在正常與糖尿病小鼠體內組織間,鉻元素的運送與血糖及胰島素反應有關,然而其機制仍未明瞭。我們首先在C57BL/6J雄性小鼠,利用飲食誘導肥胖模式以模擬人類肥胖症,將C57BL6J小鼠分別餵食正常5001標準飼糧與高油脂飼糧12週,比較正常與肥胖小鼠體內組織間,鉻元素分布變化與能量代謝異常之影響。其次是將誘導肥胖且具代謝症候群之C57BL6J小鼠與KK/HlJ糖尿病小鼠,腹腔注射高劑量類固醇(Prednisolone 2 mg/kg body weight),測量24小時後其體內組織鉻元素、胰島素阻抗指數(HOMA-IR)、禁食血糖、禁食三酸甘油脂、胰島素與瘦體素濃度之變化。本研究以飲食誘導肥胖模式(Diet-Induced Obesity, DIO),可成功誘發出高三酸甘油脂、高血糖、高胰島素血症、肥胖等代謝症候群症狀。研究結果說明高劑量prednisolone會導致主要的胰島素敏感組織如肝臟、肌肉與脂肪鉻含量顯著下降,而股骨鉻含量則顯著上升,並導致醣類與脂質代謝異常,尤其是在高脂飲食的效果更為顯著。本研究發現肥胖會強化促進prednisolone造成體內組織間鉻元素之移動,進一步造成肝臟、肌肉與脂肪組織鉻元素下降,最終導致葡萄糖與脂質代謝異常。
Obesity is a major risk factor for the development of insulin resistance, type 2 diabetes mellitus (DM) and coronary heart disease. It is now clear that obesity promotes the development of metabolic syndrome (Syndrome X) and type 2 DM. In clinical medical studies of human and experimental animals, long-term use of glucocorticoids could lead to symptoms of the metabolic syndrome, including obesity, insulin resistance, glucose intolerance and hyperglycemia. Trivalent chromium has proven to be a cofactor for insulin action, it facilitates the movement of glucose into cells, enhances insulin binding to insulin receptors, and improves glucose disposal for prevention of type 2 DM. Based on animal and preliminary human studies, steroid-induced diabetes can be reversed by chromium supplementation. In 2004, Coldfelder et al indicated that the transportation and distribution of chromium were altered in response to the increases serum glucose or insulin in both normal and diabetic mice however, the mechanisms of chromium transportation are still unknown. Here, we used diet-induced obesity (DIO) model to mimic human obesity in C57BL/6J male mice. C57BL/6J male mice were divided into normal chow diet and high-fat diet groups and fed for 12 weeks before the body chromium distribution and abnormality in energy metabolism were compared. Our second study was to investigate body chromium distribution, insulin resistance index (HOMA-IR), fasting serum glucose level, fasting serum triglyceride level as well as serum insulin and leptin levels 24hrs after a bolus intraperitoneal injection (2mg/kg) of prednisolone to obese C57BL/6J mice with metabolic syndrome and KK/HlJ type 2 diabetic mice. The results indicated a successful induction of metabolic syndrome by DIO model, promoting hypertriglyceridemia, hyperglycemia, hyperinsulinemia and obesity in C57BL/6J and KK/HlJ mice. Single dose of prednisolone significantly decreased chromium concentration in insulin-sensitive tissues such as liver, fat and skeletal muscle but chromium concentration in femoral bone was significantly increased; which lead to abnormality of glucose/lipid metabolism. This alteration of chromium distribution and glucose metabolism was especially prominent in high-fat diet group. In conclusion, the study strongly suggested that obesity could enhance the movement of chromium distribution induced by a bolus dose of 2 mg/kg of prednisolone which ultimately lead to abnormal glucose and lipid metabolism.
第一章、緒言…………………………………………………..…………. 01
第二章、文獻探討…………………………………………...…………… 03
第一節 糖尿病之簡介………………………………..……...………... 03
一、全球糖尿病的現況…………………………....…………..…… 03
二、糖尿病的定義與病因………………….………………..……… 04
三、糖尿病的分類與診斷………………………..…..……..……… 07
四、台灣糖尿病的流行病學………………….………………..…… 09
第二節 胰島素訊息傳導與作用………….……………………..…… 10
一、胰島素…………………………………….………..…………… 10
二、胰島素受體………………………………...…………………… 11
三、胰島素受體基質………………………..….……..…………… 12
四、磷酸肌醇 3’-激酶………...............................…..…................... 12
五、Protein tyrosine phosphatase………………….………………… 13
六、PTEN/SHIP2……………………………..…………………… 13
七、Akt (protein kinase B)…………………….……....….………… 14
八、葡萄糖轉運蛋白……………………..……..….……………… 14
第三節 葡萄糖皮質固醇…………………………..…....……………… 16
一、Prednisolone之簡介………..………………...…..……..……… 16
二、腎上腺葡萄糖皮質激素合成...……………….....…...………… 17
三、葡萄糖皮質固醇與胰島素阻抗………..………..…..………… 19
第四節 微量元素 - 鉻 (Chromium)…………………….…….…….… 20
一、鉻之背景與生化特性………………………..…….…….…… 20
二、鉻與胰島素阻抗及葡萄糖耐受性不良……………..…..…… 21
三、鉻對糖尿病之預防及控制……………………..…..………… 23
1、鉻與第一型糖尿病…………………………...…..….………… 23
2、鉻與第二型糖尿病………………………….…...….………… 24
3、鉻與類固醇性糖尿病……………………...….….…………… 25
4、鉻與妊娠性糖尿病…………………………...…….………… 27
四、鉻的作用機制…………………………………...….………… 27
1、耐糖因子………………………………………...….….……… 28
2、砒碇甲酸鉻………………………………...…………....……… 30
3、低分子量鉻結合物…………………...………………..…..…… 33
第五節 糖尿病與胰島素阻抗之動物模式……………..…..………..… 36
第六節 肥胖與胰島素阻抗………………………….……….……....… 39
一、瘦體素對肥胖與胰島素阻抗…………..………………....…… 40
第三章、材料與方法………………………………...…………….……… 41
第一節 實驗動物………………………………...………..…….……… 41
實驗一、不同能量飲食效應對於C57BL/6J雄性小鼠體內鉻
元素變化與能量代謝之研究……………………….………...… 41
實驗二、一針高劑量prednisolone 對餵食5001標準飼料C57BL/6J雄性小鼠體內組織鉻元素變化與能量代謝之研究....…..…..…. 43
實驗三、一針高劑量prednisolone 對於高油脂飲食之C57BL/6J雄性小鼠體內組織鉻元素變化與能量代謝之影響....…....…….…… 44
實驗四、一針高劑量prednisolone 對於KK雄性小鼠體內組織鉻元素變化與禁食血糖值之影響…………………………..…..….… 45
第二節 樣本分析………………………...………………….………… 46
一、血糖濃度分析……………………………...........…..…..……… 46
二、三酸甘油脂濃度分析..…………..…........….….….…….……… 46
三、傳統硝酸消化法………………………………...…..…..……… 47
四、石墨爐式原子吸收光譜儀…………...…………..…..………… 48
五、酵素免疫分析法分析胰島素與瘦體素…………..…..…...…… 50
六、HOMA之分析分法…………………..…………..…………… 51
七、統計分析……………………………...……………..…..……… 51
第四章、結果…………………………………………...……….………… 52
實驗一、不同能量飲食效應對於C57BL/6J雄性小鼠體內鉻元素變化與能量代謝之研究………………………………..…..……… 52
實驗二、一針高劑量prednisolone 對餵食5001標準飼料C57BL/6J雄性小鼠體內組織鉻元素變化與能量代謝之研究..….…….…. 57
實驗三、一針高劑量prednisolone 對於高油脂飲食之C57BL/6J雄性小鼠體內組織鉻元素變化與能量代謝之影響.....……….…..…. 60
實驗四、一針高劑量prednisolone 對於KK雄性小鼠體內組織鉻元素變化與禁食血糖值之影響………………………….………… 63
第五章、討論……………………………………….……………………... 67
第六章、結論……………………………………………….……………... 76
參考文獻……………………………………………………….…………... 77
附錄………………………………………………………….……………... 97
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