Promoting insulin secretion in pancreatic, islets by means of bisphenol A and nonylphenol via intracellular estrogen receptors
Promoting insulin secretion in pancreatic, islets by means of bisphenol A and nonylphenol via intracellular estrogen receptors
复制标题
DOI：
10.1016/j.fct.2005.01.009
复制
发表时间：
2005-05-01
影响因子：
4.3
通讯作者：
Tsuda, K
中科院分区：
文献类型：
--
作者：
Adachi, T;Yasuda, K;Tsuda, K
本研究探讨了内分泌干扰物双酚A（BPA）和壬基酚（NP）对大鼠胰岛分泌胰岛素的影响。急性暴露于BPA和NP后，BPA和NP（0.1，1，10，100和1000 pg/l）均不影响16.7 mM葡萄糖浓度下的胰岛素分泌。然而，长期暴露于BPA或NP在16.7 mM葡萄糖中24小时后的胰岛素分泌显著高于未暴露。为了确定长期暴露于BPA和NP导致的胰岛素分泌增加是否通过细胞内雌激素受体诱导，我们使用放线菌素-D（Act-D）（RNA合成抑制剂）和ICI 182，780（ICI）（雌激素受体抑制剂）阻断细胞溶质/核雌激素受体。在长期暴露于BPA（10 μ g/l）或NP（10 μ g/l）后，Act-D或ICI治疗消除了胰岛素分泌的促进作用。总之，我们已经证明了第一次，长期暴露于内分泌干扰物，如BPA和NP，促进体外胰岛分泌胰岛素，通过胞质/核雌激素受体。(c)2005爱思唯尔有限公司保留所有权利。
In this study, we investigated the effects of endocrine disrupters bisphenol A (BPA) and nonylphenol (NP) on insulin secretion from rat pancreatic islets. Following acute exposure to BPA and NP, neither BPA nor NP (0.1, 1, 10, 100 and 1000 pg/l) affected insulin secretion in concentrations of 16.7 mM glucose. However, insulin secretion following long-term exposure to BPA or NP for 24 h in 16.7 mM glucose was significantly higher than without exposure. To determine Whether increased insulin secretion resulting from long-term exposure to BPA and NP is induced via intracellular estrogen receptors, we blocked the cytosolic/nuclear estrogen receptors, using actinomycin-D (Act-D), an inhibitor of RNA synthesis, and ICI 182,780 (ICI), an estrogen receptor inhibitor. Following long-term exposure to BPA (10 mu g/l) or NP (10 mu g/l), Act-D or ICI treatment eliminated the facilitation of insulin secretion. In conclusion, we have demonstrated for the first time that long-term exposure to endocrine disrupters, such as BPA and NP, promotes in vitro insulin secretion from the pancreatic islets, via cytosolic/nuclear estrogen receptors. (c) 2005 Elsevier Ltd. All rights reserved.