中文摘要：

背景到丰满的酸的胰腺的房间的延长暴露增加基础胰岛素分泌物，但是禁止刺激葡萄糖的胰岛素分泌物。Rosiglitazone 是 thiazolidinediones 的一个新 antidiabetic 代理人。然而，在 thiazolidinediones 之间的关系和胰岛素分泌物是高度争论的。这研究的目的是在长期的暴露下面在小岛的胰岛素分泌物上探索 rosiglitazone 的效果和机制到免费的丰满的酸(船边交货).Methods 胰腺的小岛被 collagenase 消化并且由葡聚糖坡度 centrifugation 方法从男 Sprague-Dawley 老鼠的 pancreata 孤立。净化的小岛当面是有教养的或为 48 个小时的 rosiglitazone 和 palmitate 的缺席。胰岛素分泌物被放射性免疫测定测量。peroxisome 的 mRNA 水平激活 proliferator 的受体(，解开蛋白质 2 (UCP-2 ) 并且胰岛素被即时聚合酶链反应(PCR ) 决定。房间 cytotoxicity 试金被数 kit-8 的房间测量。暴露于提高的 palmitate 48 个小时的结果小岛出现了一增加基础并且减少的刺激葡萄糖的胰岛素分泌物(P < 0.01 ) 。UCP-2 的 mRNA 水平被 3.7 褶层在 palmitate 的 0.5 mmol/L 集中增加。当小岛面对 rosiglitazone (1.0 mol/L ) 与 palmitate (0.5 mmol/L ) 是有教养的时，基础、刺激葡萄糖的胰岛素分泌物逆行到控制小岛的一个模式(P < 0.05， P < 0.01 ) 。在文化媒介的 rosiglitazone 的增加减少了由 2.2 褶层的 UCP-2 的 mRNA 水平，有统计上重要的差别(P < 0.05 ) 作为与与 palmitate 有教养的小岛相比独自一个。房间生存能力没被影响。在到 palmitate 的长期的暴露下面的孤立的胰腺的小岛的胰岛素分泌物上的 rosiglitazone 的保护的效果可能通过 UCP-2 表示的 downregulation 被调停的结论。

英文摘要：

Background Prolonged exposure of pancreatic β-cells to fatty acids increases basal insulin secretion but inhibits glucose-stimulated insulin secretion. Rosiglitazone is a new antidiabetic agent of the thiazolidinediones. However, the relationship between thiazolidinediones and insulin secretion is highly controversial. The aim of this study is to explore the effect and mechanism of rosiglitazone on insulin secretion of islets under chronic exposure to free fatty acids （FFA）. Methods Pancreatic islets were isolated from the pancreata of male Sprague-Dawley rats by the collagenase digestion and by the dextran gradient centrifugation method. The purified islets were cultured in the presence or absence of rosiglitazone and palmitate for 48 hours. The insulin secretion was measured by radioimmunoassay. The mRNA level of peroxisome proliferator-activated receptor y, uncoupling protein 2 0dCP-2） and insulin were determined by real-time polymerase chain reaction （PCR）. The cell cytotoxicity assay was measured by cell counting kit-8. Results Islets exposed to elevated palmitate for 48 hours showed an increased basal and a decreased glucose-stimulated insulin secretion （P〈0.01）. The mRNA level of UCP-2 was increased by 3.7 fold in the 0.5 mmol/L concentration of palmitate. When islets were cultured with palmitate （0.5 mmol/L） in the presence of rosiglitazone （1.0 pmol/L）, both basal and glucose-stimulated insulin secretion reversed to a pattern of control islets （P〈0.05, P〈0.0 1）. The addition of rosiglitazone in the culture medium decreased the mRNA level of UCP-2 by 2.2 fold, having a statistically significant difference （P〈0.05） as compared with islets cultured with palmitate alone. The cell viability was not affected. Conclusion The protective effects of rosiglitazone on insulin secretion of isolated pancreatic islets under chronic exposure to palmitate might be mediated through the downregulation of UCP-2 expression.