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題名 | 大蒜精油對於HIT-T15細胞胰島素分泌功能之影響=The Effect of Garlic Oil on Insulin Secretion in HIT-T15 Cells |
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作者姓名(中文) | 王奕雯; 李宗貴; 沈立言; 劉承慈; | 書刊名 | 臺灣營養學會雜誌 |
卷期 | 36:4 2011.12[民100.12] |
頁次 | 頁125-135 |
分類號 | 411.3 |
關鍵詞 | HIT-T15細胞株; 大蒜精油; 胰島素; 葡萄糖刺激之胰島素分泌作用; 葡萄糖轉運蛋白; HIT-T15 cell line; Garlic oil; Insulin; Glucose-stimulated insulin secretion; GSIS; Glucose transporter; ATP; |
語文 | 中文(Chinese) |
中文摘要 | 已知葡萄糖毒性抑制胰島素分泌,本研究觀察大蒜精油(GO)對於胰島戶細胞株胰島素分泌功能之影響。HIT-T15細胞預培養於合不同葡萄糖濃度(5.5、11.1或33.3 mM)之培養液中,並加入不同濃度GO(1-100 μg/ml),24小時後觀察細胞存活率、培養液中胰島素含量,清洗細胞後,另以葡萄糖刺激胰島素分泌。預培養於高糖濃度之細胞,亦觀察GO對於其氧化壓力指標之影響。結果發現,在預培養時添加GO(1-10 μg/ml),增加培養液中胰島素含量,且效果與glibenclamide相當,且也增加葡萄糖刺激細胞分泌胰島素之作用,並伴隨胞內ATP含量增加、葡萄糖運輸系統Km值降低及Vmax值增加。高糖顯著增加細胞脂質過氧化程度,並顯著降低細胞超氧歧化酶(SOD)活性,但是不影響總穀胱甘肽(GSH)含量或穀胱甘肽過氧化酶(GPx)與穀胱甘肽還原酶(GR)活性。高糖下添加GO雖然增加細胞SOD活性,但未改善細胞脂質過氧化程度。由結果得知,不論基礎或高糖濃度下,GO均促進HIT-T15細胞胰島素分泌作用,其機制與增加細胞葡萄糖利用率有關,但可能與降低高糖所致之氧化傷害無關。 |
英文摘要 | It is known that glucose toxicity suppresses insulin secretion. Using an islet β cell line (HIT-T15), the present study investigated the effect of garlic oil (GO) on insulin secretion. Cells were pre-cultured in various concentrations of glucose (5.5, 11.1, and 33.3 mM) with or without GO (1~100 μg/ml) for 24 h followed by the determination of cell validity and insulin secretion in the pre-culture. After washing cells after the pre-culture, glucose-stimulated insulin secretion (GSIS), the cellular ATP content, and glucose transport kinetics were determined. The effect of GO on the oxidative condition of cells cultured under a hyperglycemic condition was also investigated. It was found that GO (1~10 μg/ml) improved insulin secretion of cells in the pre-culture medium to a level similar to that of glibenclimide; it also improved the GSIS in association with elevated cellular ATP, decreased Km, and increased Vmax of the glucose transport system. Hyperglycemia increased thiobarbituric acid reactive substances (TBARS) level and decreased superoxide dismutase (SOD) activity in cells, although the total glutathione (GSH) content, the activities of glutathione peroxidase (GPx) and glutathione reductase (GR) remained unaffected. GO improved SOD activity of cells cultured under a hyperglycemic condition; however, it did not ameliorate the increase in TSARS in these cells. In conclusion, GO acutely improved GSIS in the HIT-T15βcell line cultured under normal and hyperglycemic conditions which was associated with increased glucose utilization by these cells but not through an antioxidant effect. |
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