本文關(guān)鍵詞： 非諾貝特 老年高脂喂養(yǎng)C小鼠 β細(xì)胞功能 鈣離子　出處：《中國(guó)臨床藥理學(xué)雜志》2015年10期 　論文類型：期刊論文

【摘要】：目的考察非諾貝特對(duì)老年高脂喂養(yǎng)C57(Aged-C57)小鼠胰島β細(xì)胞功能的影響并探討可能的作用機(jī)制。方法老年高脂喂養(yǎng)C57小鼠(n=28),隨機(jī)分為老年動(dòng)物模型組和非諾貝特組(100 mg·kg-1d-1),連續(xù)灌胃給藥8周。另取正常雄性C57小鼠14只,作為正常組。考察其對(duì)血糖、血脂、胰島素敏感性及β細(xì)胞功能的影響。結(jié)果非諾貝特給藥約5周,可顯著改善Aged-C57小鼠胰島素耐量血糖-時(shí)間曲線下面積(P0.01);給藥7周,能顯著降低Aged-C57小鼠的空腹血糖(P0.01)及空腹血胰島素水平(P0.05);亦可顯著降低其血清三酰甘油水平(P0.05);非諾貝特可顯著增加高血糖鉗夾葡萄糖刺激后5min和10 min的胰島素分泌(P0.01,P0.05),增加穩(wěn)態(tài)葡萄糖輸注速率(P0.05);非諾貝特可明增加其胰腺中Ca2+含量(P0.05)及胰腺線粒體ATPase活性(P0.01);與模型組相比,非諾貝特可顯著上調(diào)胰腺中胰島素合成和信號(hào)通路中INS1、PDX1、IRS2和PKB的mRNA表達(dá)水平(P0.01),顯著上調(diào)鈣離子釋放相關(guān)蛋白R(shí)YR3及SERCA2的基因表達(dá)水平(P0.001,P0.01)。結(jié)論長(zhǎng)期給予非諾貝特顯著改善老年高脂喂養(yǎng)C57(Aged-C57)小鼠的糖脂代謝紊亂狀態(tài),其作用機(jī)制可能與通過上調(diào)胰腺PDX1、INS1及細(xì)胞鈣庫(kù)Ca2+釋放相關(guān)因子的表達(dá)有關(guān)。
[Abstract]:Objective to investigate the effect of fenofibrate on the function of islet 尾 cells in aged C57Aged-C57mice and to explore the possible mechanism. Methods the aged C57 mice were randomly divided into aged animal model group and fenofibrate group (100 mg 路kg ~ (-1) d ~ (-1)). For 8 weeks, 14 normal male C57 mice were taken. As a normal group, the effects of fenofibrate on blood glucose, blood lipids, insulin sensitivity and 尾 -cell function were investigated. Results fenofibrate administration for about 5 weeks significantly improved the area under the insulin tolerance glycemic time curve in Aged-C57 mice (P 0.01), and administered it for 7 weeks. It can significantly decrease fasting blood glucose (P0.01) and fasting serum insulin level (P0.05N) and serum triglyceride level (P0.05N) in Aged-C57 mice. Fenofibrate can significantly increase insulin secretion at 5 minutes and 10 min after hyperglycemic clamp glucose stimulation. In comparison with the model group, the stable glucose infusion rate (P0.05) and the content of Ca2 in the pancreas (P0.05) and the activity of mitochondrial ATPase in the pancreas were increased by P0.01 (P0.05), and compared with the model group, compared with the model group, the content of Ca2 in the pancreas and the activity of mitochondrial ATPase in the pancreatic mitochondria were increased. Fenofibrate could significantly upregulate insulin synthesis in pancreas and mRNA expression level of PKB and IRS2 in the signal pathway of INS1PDX1, and significantly up-regulate the gene expression level of Ca2 + releasing related protein RYR3 and SERCA2. Conclusion fenofibrate can be significantly modified by fenofibrate for a long time. The disorder of glucose and lipid metabolism in C57 + Aged-C57 mice. The mechanism may be related to the up-regulation of the expression of PDX1-INS1 and Ca2 release in the calcium pool of the pancreas.
【作者單位】： 中國(guó)醫(yī)學(xué)科學(xué)院北京協(xié)和醫(yī)學(xué)院藥物研究所天然藥物活性物質(zhì)與功能國(guó)家重點(diǎn)實(shí)驗(yàn)室;
【基金】：國(guó)家科技重大新藥創(chuàng)制、重大專項(xiàng)基金資助項(xiàng)目(2012ZX09301002-004)
【分類號(hào)】：R965

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