中国综合临床
中國綜閤臨床
중국종합림상
CLINICAL MEDICINE OF CHINA
2012年
12期
1276-1279
,共4页
闫明先%赵华清%王亚茹%李晓荣%杨静%王文奇%王义国
閆明先%趙華清%王亞茹%李曉榮%楊靜%王文奇%王義國
염명선%조화청%왕아여%리효영%양정%왕문기%왕의국
高脂饮食%胰腺腺泡细胞%三磷酸肌醇%外分泌%缩胆囊素
高脂飲食%胰腺腺泡細胞%三燐痠肌醇%外分泌%縮膽囊素
고지음식%이선선포세포%삼린산기순%외분비%축담낭소
High-fat diet%Pancreatic acinar cell%1,4,5-trisphosphate%Excrine%Cholecystokinin
目的 探讨高脂饮食对胰腺腺泡细胞内三磷酸肌醇( IP3)表达及淀粉酶释放的影响.方法 雄性Wistar大鼠分为高脂饮食组和正常饮食组,分别喂养4周,全自动生化仪检测血液甘油三酯、胆固醇、淀粉酶和葡萄糖浓度,并观察胰腺病理组织学变化.两组大鼠分离并培养胰腺腺泡细胞,应用[3H]-IP3检测试剂盒检测细胞内IP3浓度;并应用胆囊收缩素(CCK)-8对腺泡细胞刺激培养,检测两组大鼠腺泡细胞淀粉酶释放率.结果 高脂饮食大鼠出现高脂血症,其胰腺组织病理染色发现腺泡细胞空泡化,腺泡细胞周围淋巴细胞浸润.高脂饮食大鼠的腺泡细胞IP3含量明显高于正常大鼠[(31.807±3.448) pmol/106 cells与(24.632±3.649) pmol/106 cells,t=7.479,P<0.001];且高脂饮食大鼠较正常组大鼠的腺泡细胞在不同浓度CCK-8(0.01 nmol/L和1 nmol/L)刺激下的淀粉酶释放率均明显增高[(11.056±3.369)%与(7.354±2.181)%;t=3.912,P<0.001;(13.854±4.087)%与(9.432±2.477)%,t=3.939,P<0.001).高脂饮食组大鼠的腺泡细胞IP3含量和CCK-8(1 nmol/L)刺激下的淀粉酶释放率呈正相关性(r=0.896,P<0.001).结论 长期高脂血症引起大鼠腺泡细胞对CCK刺激的外分泌敏感性增加,IP3作为信号分子具有重要作用.
目的 探討高脂飲食對胰腺腺泡細胞內三燐痠肌醇( IP3)錶達及澱粉酶釋放的影響.方法 雄性Wistar大鼠分為高脂飲食組和正常飲食組,分彆餵養4週,全自動生化儀檢測血液甘油三酯、膽固醇、澱粉酶和葡萄糖濃度,併觀察胰腺病理組織學變化.兩組大鼠分離併培養胰腺腺泡細胞,應用[3H]-IP3檢測試劑盒檢測細胞內IP3濃度;併應用膽囊收縮素(CCK)-8對腺泡細胞刺激培養,檢測兩組大鼠腺泡細胞澱粉酶釋放率.結果 高脂飲食大鼠齣現高脂血癥,其胰腺組織病理染色髮現腺泡細胞空泡化,腺泡細胞週圍淋巴細胞浸潤.高脂飲食大鼠的腺泡細胞IP3含量明顯高于正常大鼠[(31.807±3.448) pmol/106 cells與(24.632±3.649) pmol/106 cells,t=7.479,P<0.001];且高脂飲食大鼠較正常組大鼠的腺泡細胞在不同濃度CCK-8(0.01 nmol/L和1 nmol/L)刺激下的澱粉酶釋放率均明顯增高[(11.056±3.369)%與(7.354±2.181)%;t=3.912,P<0.001;(13.854±4.087)%與(9.432±2.477)%,t=3.939,P<0.001).高脂飲食組大鼠的腺泡細胞IP3含量和CCK-8(1 nmol/L)刺激下的澱粉酶釋放率呈正相關性(r=0.896,P<0.001).結論 長期高脂血癥引起大鼠腺泡細胞對CCK刺激的外分泌敏感性增加,IP3作為信號分子具有重要作用.
목적 탐토고지음식대이선선포세포내삼린산기순( IP3)표체급정분매석방적영향.방법 웅성Wistar대서분위고지음식조화정상음식조,분별위양4주,전자동생화의검측혈액감유삼지、담고순、정분매화포도당농도,병관찰이선병리조직학변화.량조대서분리병배양이선선포세포,응용[3H]-IP3검측시제합검측세포내IP3농도;병응용담낭수축소(CCK)-8대선포세포자격배양,검측량조대서선포세포정분매석방솔.결과 고지음식대서출현고지혈증,기이선조직병리염색발현선포세포공포화,선포세포주위림파세포침윤.고지음식대서적선포세포IP3함량명현고우정상대서[(31.807±3.448) pmol/106 cells여(24.632±3.649) pmol/106 cells,t=7.479,P<0.001];차고지음식대서교정상조대서적선포세포재불동농도CCK-8(0.01 nmol/L화1 nmol/L)자격하적정분매석방솔균명현증고[(11.056±3.369)%여(7.354±2.181)%;t=3.912,P<0.001;(13.854±4.087)%여(9.432±2.477)%,t=3.939,P<0.001).고지음식조대서적선포세포IP3함량화CCK-8(1 nmol/L)자격하적정분매석방솔정정상관성(r=0.896,P<0.001).결론 장기고지혈증인기대서선포세포대CCK자격적외분비민감성증가,IP3작위신호분자구유중요작용.
Objective To investigate the effects of high-fat diet on pancreatic acinar cells' IP3 expression and CCK-induced amylase release in rats.Methods Male Wistar rats were divided into high-fat diet group and normal diet group,they were fed for 4 weeks.Blood triglycerides,cholesterol,amylase and glucose levels were determined by automatic biochemical analyzer.Pancreatic tissues were taken for histopathological observations.Pancreatic acinar cells were isolated and cultured,and intracellular inositol 1,4,5-trisphosphate (IP3) was detected using a commercial kit.Amylase release rates were measured after CCK-8 stimulation.Results The rats in high-fat diet group appeared hyperlipidemia,vacuolization of acinar cells and the lymphocytes appeared around the acinar cells can be seen on the pancreatic tissue pathology staining.The levels of IP3 in acinar cells of rats fed a high-fat diet were higher than that of normal rats [(31.807 ± 3.448) pmol/106 cells vs (24.632 ± 3.649) pmol/106 cells,t=7.479,P<0.001];and amylase release rate in these rats'acinar cells were also higher than those of normal rats [when CCK-8=0.01 nmol/L:( 11.056 ±3.369)% vs (7.354 ± 2.181) %,t=3.912,P<0.001;when CCK-8=1 nmol/L:( 13.854 ± 4.087 ) % vs (9.432 ±2.477) %,t=3.939,P<0.001 ) after CCK-8 stimulation in different concentrations.Additionally,there was a positive co-relationship between acinar cell's IP3 level and amylase release (r=0.896,P<0.001 ).Conclusion Chronic high-fat diet induces hypersensitivity for pancreatic acinar cells' exocrine function,and IP3 as a signal molecule may play an important role in this process.