Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/13321
標題: 咖啡因與高脂飲食對C57BL/6JNarl小鼠血糖、Akt活性與鉻元素含量之影響
Effects of Caffeine and High-Fat Diet on Blood Glucose, Akt Activity and Chromium Contents in C57BL/6JNarl Mice
作者: 林自強
Lin, Tzu-Chiang
關鍵字: Caffeine;咖啡因;High fat diet;Blood glucose;Akt;Chromium;高脂飲食;血糖;Akt;鉻
出版社: 獸醫學系暨研究所
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摘要: 
由於咖啡因與高脂飲食皆會導致血糖上升,而血糖上升會刺激胰島素的分泌,藉由胰島素之作用,可促使血糖進入細胞,因此,本研究探討咖啡因與高脂飲食於細胞內之交互作用。實驗使用低脂及高脂飼糧飼養之C57BL/6JNarl小鼠,探討咖啡因對血糖及Akt活性之影響。結果顯示,高脂飼糧導致小鼠脂肪組織增加並產生高血糖現象,且組織中Akt總量顯著增加,但Akt-pSer473卻減少,特別是肌肉組織。在給予咖啡因後,高脂組小鼠血糖上升更為顯著,且肝臟及脂肪組織中Akt-pSer473顯著增加,但在肌肉組織中之效果卻有限。此意謂著高脂飲食阻礙了肌肉組織Akt的活化,然而肝臟及脂肪組織則不受影響。此外,咖啡因會造成高脂組血糖急劇上升,所以高脂飲食及肥胖的個體需注意咖啡因的攝取。前人研究發現鉻元素可輔助胰島素作用及改善第二型糖尿病的症狀,本研究結果顯示,咖啡因會造成高脂組小鼠肝臟、肌肉及脂肪組織中鉻含量顯著減少,然而正常飼糧組小鼠則無顯著的影響。因此推論,高脂飲食造成鉻元素於肌肉組織內的減少或許與Akt的不活化有關。

Since caffeine and high-fat diet both can cause blood glucose increase and insulin secretion, and insulin can help blood glucose to get into cells. Therefore, this study was aimed to investigate the intracellular interaction between caffeine and high-fat diet. C57BL/6JNarl mice were fed on low-fat and high-fat diet to evaluate effects of caffeine on blood glucose and Akt activity. Results indicated that body fat, blood glucose and total Akt were significantly increased in high-fat diet (HFD) group. However Akt-pSer473 did not increased, especially in muscle tissue. After caffeine injection, blood glucose concentrations were spiking higher in HFD group and Akt-pSer473 contents were also increased in liver and fat, but not in muscle. It seems that high-fat diet blocks Akt activation in muscle, but not in liver and fat tissue. It is suggested that the obese subjects should be careful about caffeine uptake to avoid blood glucose spiking. Chromium is known can help insulin function in type 2 diabetic subjects. After caffeine injection, it was found that chromium in metabolic tissue is significantly lowered in HFD group, but not in normal diet group. It is suggested that the muscle chromium decreasing in HFD group's tissue may impede the Akt activation.
URI: http://hdl.handle.net/11455/13321
其他識別: U0005-0208200709501000
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