中华糖尿病杂志
中華糖尿病雜誌
중화당뇨병잡지
CHINES JOURNAL OF DLABETES MELLITUS
2009年
2期
94-97
,共4页
崔雅菁%刘洋%李宏亮%潘琳%刘雪丽%杨文英%萧建中
崔雅菁%劉洋%李宏亮%潘琳%劉雪麗%楊文英%蕭建中
최아정%류양%리굉량%반림%류설려%양문영%소건중
胰岛素%代谢%β细胞%二氮嗪
胰島素%代謝%β細胞%二氮嗪
이도소%대사%β세포%이담진
Insulin%Metabolism%Beta cells%Diazoxide
目的 用二氮嗪干预高脂喂养大鼠,探讨抑制胰岛素过度分泌对大鼠脂肪代谢和胰岛β细胞功能的影响.方法 2007年5月至2008年7月,10周龄雄性SD大鼠30只按随机数字表法分为正常对照组(n=10,给予普通饲料)、高脂喂养组(n=10,给予高脂饲料)及二氮嗪组(n=10,给予高脂饲料+30 mg·kg-1·d-1二氮嗪).干预8周后,行腹腔注射葡萄糖耐量试验,测定血清甘油三酯和游离脂肪酸浓度以及肝脏和肌肉中甘油三酯含量,通过聚合酶链反应观测关键脂代谢基因的表达水平.多组间差异比较采用单因素方差分析及Student-Newman-Kewls检验.结果 腹腔注射匍萄糖耐量试验显示:高脂喂养组胰岛素曲线下总面积低于正常对照组(分别为624±83和919±145),二氮嗪干预后明显增加(2220±383;F=15.73,P<0.01).高脂喂养组血清甘油三酯和游离脂肪酸浓度以及肌肉和肝脏中甘油三酯含量明显增加,肝脏呈中至重度脂肪变,二氮嗪干预可明显逆转这些变化.高脂喂养组肝脏ACC1 mRNA表达增加,二氮嗪干预可明显逆转这一变化(F=3.71,P<0.05).高脂喂养组肝脏和肌肉CPT1 mRNA表达增加,二氮嗪可促进这一变化(分别为F=3.61,P<0.05;F=4.93,P<0.05).结论 二氮嗪可抑制胰岛素过度分泌,保护胰岛β细胞,还可能通过改变肝脏及肌肉脂肪代谢减轻脂肪堆积,降低血清甘油三酯和游离脂肪酸水平.
目的 用二氮嗪榦預高脂餵養大鼠,探討抑製胰島素過度分泌對大鼠脂肪代謝和胰島β細胞功能的影響.方法 2007年5月至2008年7月,10週齡雄性SD大鼠30隻按隨機數字錶法分為正常對照組(n=10,給予普通飼料)、高脂餵養組(n=10,給予高脂飼料)及二氮嗪組(n=10,給予高脂飼料+30 mg·kg-1·d-1二氮嗪).榦預8週後,行腹腔註射葡萄糖耐量試驗,測定血清甘油三酯和遊離脂肪痠濃度以及肝髒和肌肉中甘油三酯含量,通過聚閤酶鏈反應觀測關鍵脂代謝基因的錶達水平.多組間差異比較採用單因素方差分析及Student-Newman-Kewls檢驗.結果 腹腔註射匍萄糖耐量試驗顯示:高脂餵養組胰島素麯線下總麵積低于正常對照組(分彆為624±83和919±145),二氮嗪榦預後明顯增加(2220±383;F=15.73,P<0.01).高脂餵養組血清甘油三酯和遊離脂肪痠濃度以及肌肉和肝髒中甘油三酯含量明顯增加,肝髒呈中至重度脂肪變,二氮嗪榦預可明顯逆轉這些變化.高脂餵養組肝髒ACC1 mRNA錶達增加,二氮嗪榦預可明顯逆轉這一變化(F=3.71,P<0.05).高脂餵養組肝髒和肌肉CPT1 mRNA錶達增加,二氮嗪可促進這一變化(分彆為F=3.61,P<0.05;F=4.93,P<0.05).結論 二氮嗪可抑製胰島素過度分泌,保護胰島β細胞,還可能通過改變肝髒及肌肉脂肪代謝減輕脂肪堆積,降低血清甘油三酯和遊離脂肪痠水平.
목적 용이담진간예고지위양대서,탐토억제이도소과도분비대대서지방대사화이도β세포공능적영향.방법 2007년5월지2008년7월,10주령웅성SD대서30지안수궤수자표법분위정상대조조(n=10,급여보통사료)、고지위양조(n=10,급여고지사료)급이담진조(n=10,급여고지사료+30 mg·kg-1·d-1이담진).간예8주후,행복강주사포도당내량시험,측정혈청감유삼지화유리지방산농도이급간장화기육중감유삼지함량,통과취합매련반응관측관건지대사기인적표체수평.다조간차이비교채용단인소방차분석급Student-Newman-Kewls검험.결과 복강주사포도당내량시험현시:고지위양조이도소곡선하총면적저우정상대조조(분별위624±83화919±145),이담진간예후명현증가(2220±383;F=15.73,P<0.01).고지위양조혈청감유삼지화유리지방산농도이급기육화간장중감유삼지함량명현증가,간장정중지중도지방변,이담진간예가명현역전저사변화.고지위양조간장ACC1 mRNA표체증가,이담진간예가명현역전저일변화(F=3.71,P<0.05).고지위양조간장화기육CPT1 mRNA표체증가,이담진가촉진저일변화(분별위F=3.61,P<0.05;F=4.93,P<0.05).결론 이담진가억제이도소과도분비,보호이도β세포,환가능통과개변간장급기육지방대사감경지방퇴적,강저혈청감유삼지화유리지방산수평.
Objective To investigate the effects of inhibition of excessive insulin secretion on lipid metabolism and beta-cell functions in high-fat feeding rats following diazoxide intervention. Methods During May 2007 and July 2008, 30 male SD rats (10-week old) were randomly divided into the normal control group (n=10; normal diet), high-fat diet group (n=10; high-fat diet), and diazoxide group (n=conducted, and serum levels of free fatty acid and triglyceride and triglycefide components in the liver or skeletal muscle were measured. Expression of ACCI mRNA and L-CPT1 mRNA was investigated using real-time polymerase chain reaction. One-way analysis of variances and Student-Newman-Kewls test were used for data analysis. Results In intra-pcritoneal glucose tolerance test, the insulin area under the curve was decreased in the high-fat diet group compared with the normal control group, while diazoxide intervention attenuated the decline (F=15.73,P<0.01). The plasma triglyceride and free fatty acid and triglyceride component in the muscles or liver were increased in the high-fat diet group, ahhough diazoxide reversed these changes. High-fat diet alone increased the expression of ACC1 mRNA in the liver, which could be prevented by diazoxide (F=3.71, P<0.05). The expression of CPT1 mRNA in the liver or muscles was induced by high-fat diet, and diazoxide enhanced this effect (F=3.61, P < 0. 05; F=4. 93, P < 0.05).Conclusions Diazoxide may inhibit excessive insulin secretion and preserve pancreatic beta-cell function.Moreover, diazoxide could improve fatty acid metabolism and reduce fat accumulation in the liver and muscles, so as to decrease plasma levels of triglyceride and free fatty acid.