Reduced cholecystokinin mediates the inhibition of pancreatic growth induced by bile salts.
Reduced cholecystokinin mediates the inhibition of pancreatic growth induced by bile salts.
复制标题
胆囊收缩素减少介导胆汁盐诱导的胰腺生长的抑制。
DOI：
10.1152/ajpgi.1990.259.1.g86
复制
发表时间：
1990
期刊：
影响因子：
--
通讯作者：
Thompson,JC
中科院分区：
文献类型：
--
作者：
Gomez,G;TownsendJr,CM;Green,DW;Rajaraman,S;GreeleyJr,GH;Thompson,JC
本文研究了鲁米那胆盐对小鼠血浆胆囊收缩素（CCK）水平和胰腺生长的影响。对照小鼠血浆CCK的非空腹水平为8.1 +/- 1.5 pM。给小鼠喂食添加0.5%（wt/wt）牛磺胆酸钠的饲料1周后，血浆CCK的非空腹水平显著降低至4.1 +/- 0.5 pM，胰腺DNA总含量降低22%，RNA降低25%，蛋白质降低24%。同时给予CCK-8（3 μ g/kg，每日3次）可完全逆转牛磺胆酸盐对胰腺生长的抑制作用。与此相反，通过喂食4%（wt/wt）考来烯胺补充饮食1周来进行内源性胆汁盐的管腔内中和，可显著升高非空腹血浆CCK水平至14.7 +/- 1.5 pM，并使胰腺DNA总含量增加34%，RNA增加40%，蛋白质增加35%。所有的刺激作用，考来烯胺对胰腺的生长完全取消了管理的高度有效的和具体的CCK受体拮抗剂L364，718（1毫克/公斤，每天两次）。因此，这些发现表明，胆盐似乎通过调节血浆CCK水平在胰腺生长中发挥生理作用。
The effects of luminal bile salts on plasma levels of cholecystokinin (CCK) and growth of the pancreas in mice were studied. Nonfasting levels of plasma CCK in control mice were 8.1 +/- 1.5 pM. Feeding mice a 0.5% (wt/wt) sodium taurocholate-supplemented diet for 1 wk significantly lowered nonfasting levels of plasma CCK to 4.1 +/- 0.5 pM and decreased the total contents of pancreatic DNA by 22%, RNA by 25%, and protein by 24%. All of the inhibitory effects of taurocholate on pancreatic growth were completely reversed by the simultaneous administration of CCK-8 (3 micrograms/kg, 3 times daily). In contrast, intraluminal neutralization of endogenous bile salts by feeding a 4% (wt/wt) cholestyramine-supplemented diet for 1 wk significantly elevated nonfasting levels of plasma CCK to 14.7 +/- 1.5 pM and increased the total contents of pancreatic DNA by 34%, RNA by 40%, and protein by 35%. All of the stimulatory actions of cholestyramine on pancreatic growth were completely abolished by the administration of the highly potent and specific CCK-receptor antagonist L364,718 (1 mg/kg, twice daily). These findings, therefore, indicate that bile salts appear to play a physiological role in pancreatic growth by regulation of plasma levels of CCK.