Regulation of protein synthesis in normal and diabetic rat pancreas by cholecystokinin.
Regulation of protein synthesis in normal and diabetic rat pancreas by cholecystokinin.
复制标题
胆囊收缩素对正常和糖尿病大鼠胰腺蛋白质合成的调节。
DOI：
10.1152/ajpgi.1981.241.2.g116
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发表时间：
1981
期刊：
影响因子：
--
通讯作者：
J. Williams
中科院分区：
文献类型：
--
作者：
M. Korc;A. Bailey;J. Williams
在正常和链脲佐菌素诱导的糖尿病大鼠的胰腺腺泡中，观察了CCK对[~3H]亮氨酸掺入蛋白质的影响。CCK的活性C端八肽CCK8在刺激消化酶分泌的浓度范围内(1×10~(-11)~1×10~(-10)M)增加[~3H]亮氨酸掺入蛋白质，较高浓度的CCK8则抑制掺入。[~3H]亮氨酸掺入刺激在糖尿病大鼠腺泡中最大，在喂养正常大鼠腺泡中居中，在禁食大鼠腺泡中最小。在所有腺泡中，抑制的程度是相似的。CCK8对糖尿病大鼠腺泡细胞有明显的刺激作用，作用时间为10min，孵育40min达到最大。卡巴胆碱可模拟CCK的刺激和抑制作用，而钙离子载体A23187仅能模拟抑制作用。胰岛素还能刺激糖尿病大鼠腺泡细胞[~3H]亮氨酸掺入，其作用与CCK的刺激作用相加。这些结果提示，生理浓度的CCK和其他胰腺促分泌剂可能参与了胰腺蛋白质合成的调节。
The effects of cholecystokinin (CCK) on [3H]leucine incorporation into protein were studied in isolated pancreatic acini from normal and streptozotocin-induced diabetic rats. CCK8, the biologically active C-terminal octapeptide of CCK, increased [3H]leucine incorporation into protein over a concentration range that stimulates digestive enzyme secretion (1 X 10(-11) to 1 X 10(-10) M); at higher concentrations, CCK8 inhibited incorporation. Stimulation of [3H]leucine incorporation was greatest in acini from diabetic rats, intermediate in acini from fed normal rats, and least in acini from fasted rats. The magnitude of inhibition was similar in all acini. A significant stimulatory effect of CCK8 in acini from diabetic rats was detected after 10 min and was maximal after 40 min of incubation. Carbachol mimicked both the stimulatory and inhibitory effects of CCK, whereas the Ca2+ ionophore A23187 mimicked only the inhibitory effects. Insulin also stimulated [3H]leucine incorporation in acini from diabetic rats, and its effects were additive to the stimulatory effect of CCK. The present findings suggest that physiological concentrations of CCK and other pancreatic secretagogues may participate in the regulation of pancreatic protein synthesis.