Gene expressions of the cholecystokinin (CCK) and CCK receptors, and regulation of pancreatic exocrine function

胆囊收缩素 (CCK) 和 CCK 受体的基因表达以及胰腺外分泌功能的调节

• 批准号: 06670596
• 负责人: MIYASAKA Kyoko
• 金额: $ 1.34万
• 依托单位: Tokyo Metropolitan Institute of Gerontology
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for General Scientific Research (C)
• 财政年份: 1994
• 资助国家: 日本
• 起止时间: 1994 至 1995
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-06670596/
• 关键词: CCK; CCK receptor; gene expression; CCK・レセプター; コレシストキニン; 膵臓; レセプター

1.The purification of CCK-Releasing Peptide (CCK-RP) is in progress.2.The high plasma CCK levels produced by pancreatic duct ligation (PL) increased CCK mRNA and PSTI-61 mRNA,and the maximal levels were observed on day 10 and 3 after PL,respectively.The CCK-A receptor mRNA decreased and reached the nadir on day 7, then recovered.Exclusion of bile-pancreatic juice (BPJ) from the intestine also produced the high plasma CCK level, and increased CCK mRNA and PSTI-61 mRNA levels.Administration of CCK antagonist reduced these increases.Administration of CCK analogue increased both CCK and PSTI-61 mRNA levels, however the increases were less that those produced by BPJ diversion.Therefore, it is suggested that not only CCK but also other factors may be involved in these regulations.When the levels of CCK,secretin and PSTI-61 mRNAs were examined 1,2,4,24 hours after BPJ diversion during 4-5 days after abdominal surgery, during which the gene expression of pancreatitis associated protein (PAP) was disappeared, the mRNA levels of CCK and secretin increased but not that of PSTI-61 mRNA.3.The levels of CCK and CCK-A,B receptor mRNAs decreased in old male rats, but not in female rats, and the changes in these mRNA levels in the intestine and the brain associated with age were variable.4.The involvement of vagal efferent nerve was more important to regulate CCK-stimulated pancreatic exocrine secretion, compared with afferent nerve function.The central administration of somatostatin inhibited pancreatic secretion produced BPJ diversion via synpathetic nerve.

1.CCK释放肽(CCK-RP)的纯化正在进行中。2.胰管结扎(PL)后血浆CCK水平升高，CCK mRNA和PSTI-61mRNA水平分别在PL后第10天和第3天达到最大值。CCK-A受体mRNA水平下降，在第7天达到最低点，然后恢复。从肠道中取出胆汁胰液(BPJ)也会产生较高的CCK水平，CCK和PSTI-61mRNA水平升高。给予CCK拮抗剂后，CCK和PSTI-61mRNA水平降低。CCK类似物可使CCK和PSTI-61mRNA水平升高在胰腺炎相关蛋白(PAP)基因表达消失的腹部手术后1、2、4、24小时，检测CCK、促胰液素和PSTI-61mRNAs的表达，发现CCK和促胰液素的mRNAs表达增加，而PSTI-61mRNAs的表达不受影响。3.老年雄性大鼠CCK和CCK-A、B受体mRNAs表达下降，雌性大鼠无明显变化。与传入神经功能相比，迷走传出神经的参与对CCK刺激的胰腺外分泌的调节更为重要，中枢应用生长抑素抑制胰腺分泌产生的BPJ通过交感神经转流。

项目成果

Funakoshi A: "Effect of a CCK antagonist (CR-1505) on gene expressions of cholecystokinin and secretin in rat intestine." Pancreas. 10. 118-112 (1995)

Funakoshi A：“CCK 拮抗剂 (CR-1505) 对大鼠肠道胆囊收缩素和促胰液素基因表达的影响。”

Masuda M: "Cholinergic stimulatory effect of intragastric administration of a prostaglandin E2 analogue on pancreatic exocrine secretion in conscious rats." Pancreas. 10. 395-400 (1995)

Masuda M：“胃内给予前列腺素 E2 类似物对清醒大鼠胰腺外分泌分泌的胆碱能刺激作用。”

Miyasaka K: "Changes in gene expression of cholecystokinin-A receptor after induction of pancreatitis by pancreatic duct occlusion in rats." J Gastroenterol. 30. 683-685 (1995)

Miyasaka K：“大鼠胰管闭塞诱发胰腺炎后胆囊收缩素 A 受体基因表达的变化。”

Masuda M,Tomita H,Okubo K,Miyasaka K.: "Vagal efferent nerve-dependent inhibitory action of pancreatic polypeptide and peptide YY in conscious rats : comparison with somatostatin." J Autonomic Nervous System. 50. 131-138 (1994)

Masuda M、Tomita H、Okubo K、Miyasaka K.：“胰多肽和肽 YY 在清醒大鼠中的迷走神经传出神经依赖性抑制作用：与生长抑素的比较。”

Ohta M,Tanaka Y,Masuda M,Miyasaka K,Funakoshi A.: "Impaired release of Cholecystokinin (CCK) from synaptosomes in old rats." Neurosci Lett. 198. 161-164 (1995)

Ohta M、Tanaka Y、Masuda M、Miyasaka K、Funakoshi A.：“老年大鼠突触体中胆囊收缩素 (CCK) 的释放受损。”