Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/13349
標題: Linoleicacid對大白鼠胰臟分泌胰島素之影響
Effects of Linoleic Acid on Insulin Secretion in Perfused Rat Pancreas
作者: 鄧子華
Teng, Tzu-Hua
關鍵字: linoleic acid
insulin
出版社: 獸醫學系
摘要: 在全球的糖尿病患者中,第2型糖尿病的患者就佔了90 % 以上,預計至2010年,全球會有2億以上的糖尿病患者。研究指出,飲食攝取高量的脂肪容易產生肥胖,而肥胖被認為是造成胰島素阻抗及第2型糖尿病的風險因子。相對於飽和脂肪酸有害的影響,不飽和脂肪酸不但有益於改善這些現象,也可以避免胰臟ß細胞受到飽和脂肪酸的傷害而造成細胞凋零(apoptosis)。本實驗即是以活體灌流大白鼠胰臟的模式來探討linoleic acid對大白鼠胰臟分泌胰島素之影響。首先可以發現100 µM之arachidonic acid、γ-linolenic acid、或linoleic acid皆可直接刺激胰臟分泌胰島素,亦會增強葡萄糖刺激胰島素分泌之作用。而linoleic acid在10-150 µM的濃度下,其刺激作用會與其劑量成正比。相較於正常的大白鼠,大白鼠餵飼高脂飼糧13週後,其胰臟對於linoleic acid及linoleic acid增強葡萄糖刺激胰島素分泌的反應有下降的趨勢。研究指出脂肪酸會促進核內接受器peroxisome proliferators-activated receptor(PPAR)的活性來調控代謝相關基因的轉錄。而過去的大白鼠灌流實驗發現Phosphatidylinositol-3-kinase(PI3K)抑制劑LY 294002可以消除PPAR-γ致效劑rosiglitazone刺激胰臟分泌胰島素的作用。然而實驗中顯示LY 294002並無法消除linoleic acid刺激胰臟分泌胰島素的能力,而PPAR-α抑制劑MK 886則可以抑制linoleic acid刺激胰臟分泌胰島素,亦會抑制基礎胰島素的分泌。混合兩種抑制劑一同灌流入大白鼠的胰臟後,雖然可以抑制linoleic acid刺激胰臟分泌胰島素,但是與MK 886混合linoleic acid灌流的組別並沒有顯著的差異,因此linoleic acid刺激胰島素分泌的作用係經由調控細胞內PPAR-α的活性所致。由於MK 886會抑制基礎胰島素分泌,因此活化PPAR-α在維持基礎胰島素的分泌上可能扮演著重要的角色。
People who suffered from type 2 diabetes mellitus were accounted for over 90% of the cases in the world, and it was supposed to increase gradually to 200 million in 2010 years. It was well known that intake of high-fat diet increased the risk of obesity. Obesity is an important determinant factor for the development of insulin resistance and type 2 diabetes mellitus. Contrary to the harmful effects of saturated fatty acid, unsaturated fatty acid not only improved but also prevented ß-cell from lipoapoptosis. By using rat pancreatic perfusion technique, we found that arachidonic acid, γ-linolenic acid, or linoleic acid in 100 µM stimulated insulin secretion and enhanced 10 mM glucose-induced insulin secretion. In addition, linoleic acid(10-150 µM)stimulated insulin release in a dose-dependent manner. Whereas rats fed with a high-fat diet(30%)for thirteen weeks decreased insulin secretion and glucose-stimulated insulin secretion after stimulated with 100 µM linoleic acid. Evidences shown that fatty acid regulated gene transcription by increasing the activity of nucleus receptor, peroxisome proliferators-activated receptor(PPAR). In addition, previous studies shown that phosphatidylinositol-3-kinase(PI3K)inhibitor, LY 294002, diminished the effect of PPAR-γ ligand(rosiglitazone)on insulin release. However, LY 294002 did not decrease the stimulatory effect of linoleic acid on insulin release in our experiment. Whereas the PPAR-α inhibitor, MK 886, not only inhibited the effect of linoleic acid on insulin release, but also inhibited the basal insulin secretion. The results suggested that the stimulatory effect of linoleic acid on insulin secretion might through the PPAR-α receptor. Due to the inhibitory effect of MK 886 on basal insulin secretion, the activation of PPAR-α receptor might be important for the maintenance in basal insulin secretion.
URI: http://hdl.handle.net/11455/13349
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