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스트렙토조토신 유도성 당뇨쥐의 췌장 선포세포에서 Cholecystokinin이 유도한 Calcium Signal의 변화
김명준 ( Kim Myeong Jun ),류경렬 ( Lyu Gyeong Lyeol ),성종호 ( Seong Jong Ho ),민도식 ( Min Do Sig ),이덕주 ( Lee Deog Ju ),윤신희 ( Yun Sin Hui ),한상준 ( Han Sang Jun ),조양혁 ( Jo Yang Hyeog ),김명석 ( Kim Myeong Seog ) 대한소화기학회 2003 대한소화기학회지 Vol.42 No.6
Background/Aims: Pancreatic acini of streptozotocin (STZ)-induced diabetic rats release amylase less than normal acini on cholecystokinin (CCK) stimulation. Pancreatic enzyme secretion has been closely related to the intracellular calcium concentration ([Ca2+]i) of the acinar cell. In the present study, sequential changes of the intracellular calcium signal which probably underlie the altered enzyme secretion in response to CCK-8 were investigated using pancreatic acini from diabetic rats. Methods: Diabetic rats were prepared by single intravenous injection of STZ (70 mg/kg). Stimulating experiments with CCK-8 were performed 7 days later. Pancreatic acini were isolated by collagenase digestion. Amylase release and [Ca2+]i were measured by colorimethod and calcium imaging, respectively. The geometry of intracellular calcium signal was analyzed. Results: Normal acini exhibited concentration-dependent [Ca2+]i increase and regular oscillatory calcium signal on CCK-8 stimulation. Amylase release was also concentration-dependent. However, diabetic acini showed significantly less [Ca2+]i increase, prolonged time to peak [Ca2+]i, decreased calcium spikes number, and decreased amylase release compared with normal acini. The decreased [Ca2+]i in diabetic acini was restored significantly by insulin treatment. Conclusions: Relatively decreased amylase release in diabetic pancreatic acini in response to CCK, appears to be associated with altered calcium signal due to insulin deficiency. (Korean J Gastroenterol 2003;42:519-526)