Free fatty acids induce cholecystokinin secretion through GPR120
Free fatty acids induce cholecystokinin secretion through GPR120
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DOI：
10.1007/s00210-007-0200-8
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发表时间：
2008-06-01
影响因子：
3.6
通讯作者：
Tsujimoto, Gozoh
中科院分区：
文献类型：
--
作者：
Tanaka, Toshiki;Katsuma, Susumu;Tsujimoto, Gozoh
脂肪的摄入诱导肠肽激素胆囊收缩素（CCK）的分泌;然而，负责脂质诱导的CCK释放的机制仍然未知。最近，一组游离脂肪酸（FFA）受体，其中包括长链FFA受体GPR 120和GPR 40，已被确定。在这项研究中，我们研究了这些FFA受体是否介导脂质诱导的CCK释放的小鼠。我们首先观察到，胃内给予长链游离脂肪酸增加血浆CCK水平。以小鼠肠内分泌STC-1细胞为模型，进一步研究FFA诱导CCK分泌的机制。长链游离脂肪酸促进STC-1细胞CCK的分泌，这种作用可被细胞外Ca（2+）清除或L-型Ca（2+）通道阻断剂尼卡地平所阻断。此外，这种FFA诱导的CCK分泌特异性抑制转染GPR 120特异性，但不是GPR 40特异性，短发夹RNA。这些结果表明，长链FFA通过GPR 120偶联的Ca（2+）信号诱导CCK分泌。
The ingestion of fat induces secretion of the gut peptide hormone cholecystokinin (CCK); however, the mechanism responsible for lipid-induced CCK release remains unknown. Recently, a group of free fatty acid (FFA) receptors, which includes the long-chain FFA receptors GPR120 and GPR40, has been identified. In this study, we examined whether these FFA receptors mediate lipid-induced CCK release in the mouse. We first observed that intra-gastric administration of long-chain FFAs increased plasma CCK levels. Using mouse enteroendocrine STC-1 cells as a model system, we further studied the mechanism of this FFA-induced CCK secretion. Long-chain FFAs promoted CCK secretion from STC-1 cells, which was abolished either by removal of extracellular Ca(2+)or by the L-type Ca(2+)channel blocker nicardipine. Furthermore, this FFA-induced CCK secretion was specifically inhibited by transfection of GPR120-specific, but not GPR40-specific, short hairpin RNA. These results indicate that long-chain FFAs induce CCK secretion through GPR120-coupled Ca(2+)signaling.