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首页> 外文期刊>American Journal of Physiology >Luminal CCK-releasing factor stimulates CCK release from human intestinal endocrine and STC-1 cells.
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Luminal CCK-releasing factor stimulates CCK release from human intestinal endocrine and STC-1 cells.

机译：发光的CCK释放因子刺激人肠内分泌和STC-1细胞释放CCK。

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摘要

CCK is secreted into the blood from intestinal endocrine cells following ingestion of a meal. Recently, it has been demonstrated that the ability of certain foods to stimulate CCK release is mediated by endogenously produced CCK-releasing factors. A newly discovered luminal CCK-releasing factor (LCRF) is secreted into the intestine, where it stimulates CCK secretion. However, the mechanism whereby LCRF affects intestinal epithelial cells is unknown. The current study was designed to determine whether LCRF has a direct effect on CCK cells to stimulate hormone secretion. In dispersed human intestinal mucosal cells, LCRF (5-200 nM) significantly stimulated CCK release in a concentration-dependent manner. This stimulatory effect was absent in calcium-free media and was inhibited by the L-type calcium-channel blockers diltiazem and nifedipine. To examine direct cellular effects of LCRF on CCK cells, further studies were conducted in the CCK-containing enteroendocrine cell line STC-1. As in native cells, LCRF significantly stimulated CCK release from STC-1 cells in a calcium-dependent manner. In cells loaded with a calcium-sensitive dye, LCRF stimulation produced a rapid increase in intracellular calcium. To examine the electrophysiological basis for this stimulation, whole cell recordings were made from STC-1 cells. Whole cell calcium currents were identified under basal conditions; moreover, calcium-channel activity was increased by LCRF. These studies demonstrate that 1) LCRF has a direct effect on human intestinal cells to stimulate CCK secretion, 2) stimulated hormone release is calcium dependent, and 3) LCRF activates calcium currents in CCK cells, which leads to CCK secretion.
机译：进餐后，CCK从肠内分泌细胞分泌到血液中。最近，已经证明某些食物刺激CCK释放的能力是由内源产生的CCK释放因子介导的。新发现的腔内CCK释放因子（LCRF）被分泌到肠中，在那里刺激CCK的分泌。但是，LCRF影响肠道上皮细胞的机制尚不清楚。当前的研究旨在确定LCRF是否对CCK细胞具有直接的刺激激素分泌的作用。在分散的人肠粘膜细胞中，LCRF（5-20​​0 nM）以浓度依赖性方式显着刺激CCK释放。不含钙的培养基中没有这种刺激作用，但被L型钙通道阻滞剂地尔硫卓和硝苯地平抑制了。为了检查LCRF对CCK细胞的直接细胞作用，在含CCK的肠内分泌细胞系STC-1中进行了进一步的研究。与天然细胞一样，LCRF以钙依赖性方式显着刺激SCK-1细胞释放CCK。在载有钙敏感染料的细胞中，LCRF刺激使细胞内钙迅速增加。为了检查这种刺激的电生理基础，从STC-1细胞进行了全细胞记录。在基础条件下确定全细胞钙电流;此外，LCRF增加了钙通道活性。这些研究表明，1）LCRF对人肠细胞刺激CCK分泌具有直接作用，2）刺激的激素释放是钙依赖性的，3）LCRF激活CCK细胞中的钙电流，从而导致CCK分泌。

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