GLP-1 secretion is enhanced directly in the ileum but indirectly in the duodenum by a newly identified potent stimulator, zein hydrolysate, in rats
GLP-1 secretion is enhanced directly in the ileum but indirectly in the duodenum by a newly identified potent stimulator, zein hydrolysate, in rats
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DOI：
10.1152/ajpgi.90635.2008
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发表时间：
2009-10-01
影响因子：
4.5
通讯作者：
Hara, Hiroshi
中科院分区：
文献类型：
--
作者：
Hira, Tohru;Mochida, Taisuke;Hara, Hiroshi
作者：Hira T，Mochida T，Miyashita K，Hara H.在大鼠中，GLP-1分泌在回肠中直接增强，但在十二指肠中通过新鉴定的强效刺激剂玉米醇溶蛋白水解产物间接增强。美国生理学杂志胃肠和肝脏生理学297：G663-G671，2009年。首次发表于2009年8月6日; doi：10.1152/ajpgi.90635.2008。胰高血糖素样肽-1（GLP-1）是由肠内分泌细胞（L细胞）响应食物摄入而释放的。膳食肽刺激肠道中GLP-1分泌的机制尚不清楚。在本研究中，我们发现，从玉米醇溶蛋白，一种主要的玉米蛋白[玉米醇溶蛋白水解产物（ZeinH）]制备的水解产物，强烈刺激GLP-1分泌的肠内分泌GLUTag细胞。在麻醉状态下的大鼠小肠中研究了ZeinH诱导的GLP-1分泌的刺激机制。在ZeinH施用到小肠的不同部位之前和之后通过门静脉导管收集血液。ZeinH的十二指肠、空肠和回肠给药诱导门静脉GLP-1浓度的剂量依赖性增加。响应于ZeinH回肠给药的GLP-1分泌高于十二指肠或空肠给药。辣椒素治疗食管迷走神经干废除GLP-1分泌诱导的十二指肠ZeinH，但不影响空肠或回肠ZeinH诱导的分泌。这些结果表明空肠或回肠中的ZeinH直接刺激GLP-1分泌，但十二指肠ZeinH通过迷走传入神经间接刺激GLP-1分泌。从十二指肠静脉和回肠肠系膜静脉直接采血的方法显示，ZeinH给药到结扎的十二指肠袢中增加了回肠肠系膜静脉中的GLP-1浓度，但没有增加十二指肠静脉中的GLP-1浓度。这证实了十二指肠中的ZeinH通过间接机制诱导位于回肠中的L细胞分泌GLP-1。这些结果表明，一种有效的GLP-1释放肽，ZeinH，诱导GLP-1分泌的直接和间接机制在大鼠肠道。
Hira T, Mochida T, Miyashita K, Hara H. GLP-1 secretion is enhanced directly in the ileum but indirectly in the duodenum by a newly identified potent stimulator, zein hydrolysate, in rats. Am J Physiol Gastrointest Liver Physiol 297: G663-G671, 2009. First published August 6, 2009; doi: 10.1152/ajpgi.90635.2008.-Glucagon-like peptide-1 (GLP-1) is released from enteroendocrine cells ( L cells) in response to food ingestion. The mechanism by which dietary peptides stimulate GLP-1 secretion in the gut is unknown. In the present study, we found that a hydrolysate prepared from zein, a major corn protein [zein hydrolysate (ZeinH)], strongly stimulates GLP-1 secretion in enteroendocrine GLUTag cells. Stimulatory mechanisms of GLP-1 secretion induced by ZeinH were investigated in the rat small intestine under anesthesia. Blood was collected through a portal catheter before and after ZeinH administration into different sites of the small intestine. The duodenal, jejunal, and ileal administration of ZeinH induced dose-dependent increases in portal GLP-1 concentration. GLP-1 secretion in response to the ileal administration of ZeinH was higher than that in the duodenal or jejunal administration. Capsaicin treatment on esophageal vagal trunks abolished the GLP-1 secretion induced by duodenal ZeinH but did not affect the secretion induced by jejunal or ileal ZeinH. These results suggest that ZeinH in the jejunum or ileum directly stimulates GLP-1 secretion but duodenal ZeinH indirectly stimulates GLP-1 secretion via the vagal afferent nerve. A direct blood sampling method from the duodenal vein and ileal mesenteric vein revealed that ZeinH administered into the ligated duodenal loop enhanced GLP-1 concentration in the ileal mesenteric vein but not in the duodenal vein. This confirmed that ZeinH in the duodenum induces GLP-1 secretion from L cells located in the ileum by an indirect mechanism. These results indicate that a potent GLP-1-releasing peptide, ZeinH, induces GLP-1 secretion by direct and indirect mechanisms in the rat intestine.