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  • 學位論文

分析苦瓜萃取物對腸道上皮細胞的效果 以探討可能的降血糖機制

Characterization of The Effect of Bitter Melon Extract on Intestinal Cells for the Exploration of Potential Hypoglycaemic Mechanism thereof

指導教授 : 鄭雪玲

摘要


摘要 學號 : M10518027 論文題目 :分析苦瓜萃取物對腸道上皮細胞的效果 以探討可能的降血糖機制 頁數 : 66 學校名稱 :國立屏東科技大學 所別:生物科技系 畢業日期及摘要別: 研究生 : 安妮莎 指導教授: 鄭雪玲士Harijono 論文摘要內容: 苦瓜(Momordica Charantia L.)被認為具有降血糖作用,在一些地區的傳統醫學上已經被用來治療糖尿病。然而其降糖作用的機制尚未完全了解。腸道上皮細胞在調節血糖方面有著重要的作用。腸道上皮細胞分泌與控制血糖和食慾有關的激素。此外,小腸和大腸的血糖消耗共同對降低血糖有重要作用。本研究的目的是研究苦瓜提取物對與控制血糖有關的腸道上皮細胞代謝的影響。當人類結直腸腺癌細胞株NCI-H716培養於含有苦瓜提取物的培養液時,細胞內鈣離子濃度會明顯增加,雖然胰高血糖素像是peptide-1(GLP-1)的分泌沒有增加。ELISA試驗顯示,苦瓜提取物可能刺激活化細胞的鈣離子信號通路,進而提升GLP-1分泌。同時大鼠小腸上皮細胞株IEC-18給予苦瓜提取物時,細胞不會促進葡萄糖攝取。但在胰島素阻抗性IEC-18細胞給於20 ng/ml TNF-α及 100 nM 胰島素時,細胞會促進葡萄糖攝取。在給予苦瓜提取物濃度大約50到200 ug/ml時IEC-18有不錯的促進葡萄糖吸收效果,然而BME降血糖效果不如對照組的troglitazone和rosiglitazone作用明顯。這些數據顯示,苦瓜提取物在低濃度下促進葡萄糖攝取,但不影響胰島素阻抗性IEC-18細胞中胰島素信號通路的Akt蛋白。基於此研究結果,可以得出BME可能不是胰島素增敏劑,但它可以做為胰島素的取代物。本研究的結果顯示IRS-1、Akt AS160活化的可能性; 胰島素阻抗性細胞中的PI3K抑製的可能性。 關鍵詞:苦瓜提取物、降血糖功能、血糖、intestinal L 細胞、IEC-18細胞、NCI-H716細胞。

並列摘要


ABSTRACT Student ID : M10518027 Title of Thesis : Characterization of The Effect of Bitter Melon Extract on Intestinal Cells for the Exploration of Potential Hypoglycaemic Mechanism thereof Total Pages : 66 Name of Institute : National Pingtung University of Science and Technology Name of Department : Biological Science and Technology Date of Graduation : July 2018 Degree Confered : Master Name of Student : Annisa Oktafianti Nurlatifah Advisor : Prof. Hsueh-Ling Cheng, PhD Prof. Dr. Ir. Harijono, M.App.Sc The content of this abstract in this thesis : Bitter melon (Momordica Charantia L.) has been suggested to have a hypoglycaemic effect but the underlying mechanism is not completely understood. The intestinal tissues play an important role in regulating the level of blood glucose. Whereas the effect of bitter melon on the tissues has not been characterized. The aim of this study is to investigate the effect of bitter melon extract (BME) on the metabolism of intestinal cells relating to the control of blood glucose. IEC-18 cells, a rat intestinal epithelial cell line, and NCI-H716 cells, a human intestinal enteroendocrine were used as models in this study. The results showed that BME did not affect the glucose consumption of normal IEC-18 cells, but obviously promoted the glucose uptake of insulin-resistant IEC-18 cells induced by tumor necrosis factor-α (TNF-α). The data further suggested that BME worked as an insulin substitute, but not insulin sensitizer, in insulin resistant IEC-18 cells. This affect may be mediated by the activation of AMP – activated protein kinase. Meanwhile, BME resulted in an increase in cytosolic [Ca2+] in NCI-H716 cells and promoted glucagon-like-peptide-1 (GLP-1) secretion from the cells. Overall, the data suggested that bitter melon could stimulate GLP-1 secretion from enteroendocrine cells, and promote the glucose consumption of intestinal epithelial cells. These may be part of the mechanism underlying the hypoglycaemic function thereof. Keywords : bitter melon fruit extract, hypoglycaemic function, blood glucose, bitter taste receptors, IEC-18 cells, NCI-H716 cells

參考文獻


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