中华糖尿病杂志
中華糖尿病雜誌
중화당뇨병잡지
CHINES JOURNAL OF DLABETES MELLITUS
2009年
6期
450-453
,共4页
樊大贝%秦贵军%余勤%贾贺堂%马晓君%闫晓洁
樊大貝%秦貴軍%餘勤%賈賀堂%馬曉君%閆曉潔
번대패%진귀군%여근%가하당%마효군%염효길
大麻素受体1%胰岛β细胞功能%胰岛素抵抗%肥胖大鼠
大痳素受體1%胰島β細胞功能%胰島素牴抗%肥胖大鼠
대마소수체1%이도β세포공능%이도소저항%비반대서
Cannabinoid-1 receptors%Islet beta-cell function%Insulin resistance%Obese rats
目的 研究大麻素受体1对肥胖大鼠胰岛β细胞功能的影响.方法 30只8周龄清洁级健康雄性SD大鼠,体质最150~200 g,采用数字表法随机分至正常对照组(n=6)和肥胖组(n=24).正常对照组给予普通鼠饲料喂养,肥胖组给予高脂鼠饲料喂养.8周后,与正常对照组比较,肥胖纽大鼠体质量增加36%,总胆固醇增加52%,提示24只肥胖大鼠制作成功.肥胖大鼠以数字表法随机分至生理盐水组(n=8)、WIN55212-2组(n=8)、AM251组(n=8).测定大鼠体质量、血脂、胰岛素、胰岛素原等指标,采用高葡萄糖钳央试验评价胰岛β细胞功能和胰岛素敏感性.采用LSD检验进行统计学分析.结果 腹腔注射药物2周后,生理盐水组、WIN55212-2组体质量、血脂、卒腹血糖、C肽、胰岛素、胰岛素原、胰岛素原/C肽、胰岛素原/胰岛素、胰岛素10~90 min分泌量及胰岛素最大分泌量均高于正常对照组(P<0.05),WIN55212-2组上述指标均高于生理盐水组(P<0.05),AM251组上述指标均低于生理盐水组和WIN55212-2组(P<0.05).生理盐水组、WIN55212-2组胰岛素0~10 min分泌量、匍萄糖输注率低于正常对照组(P<0.05),WIN55212-2组胰岛素0~10 min分泌量、葡萄糖输注率低于生理盐水组(P<0.05).AM251组胰岛素0~10 min分泌量、葡萄糖输注率高于生理盐水组和WIN55212-2组(P<0.05).结论 大麻素受体1受体激动可增加肥胖大鼠体质量,升高血脂水平,加重胰岛素抵抗和胰岛β细胞功能减退,抑制大麻素受体1可逆转此效应.
目的 研究大痳素受體1對肥胖大鼠胰島β細胞功能的影響.方法 30隻8週齡清潔級健康雄性SD大鼠,體質最150~200 g,採用數字錶法隨機分至正常對照組(n=6)和肥胖組(n=24).正常對照組給予普通鼠飼料餵養,肥胖組給予高脂鼠飼料餵養.8週後,與正常對照組比較,肥胖紐大鼠體質量增加36%,總膽固醇增加52%,提示24隻肥胖大鼠製作成功.肥胖大鼠以數字錶法隨機分至生理鹽水組(n=8)、WIN55212-2組(n=8)、AM251組(n=8).測定大鼠體質量、血脂、胰島素、胰島素原等指標,採用高葡萄糖鉗央試驗評價胰島β細胞功能和胰島素敏感性.採用LSD檢驗進行統計學分析.結果 腹腔註射藥物2週後,生理鹽水組、WIN55212-2組體質量、血脂、卒腹血糖、C肽、胰島素、胰島素原、胰島素原/C肽、胰島素原/胰島素、胰島素10~90 min分泌量及胰島素最大分泌量均高于正常對照組(P<0.05),WIN55212-2組上述指標均高于生理鹽水組(P<0.05),AM251組上述指標均低于生理鹽水組和WIN55212-2組(P<0.05).生理鹽水組、WIN55212-2組胰島素0~10 min分泌量、匍萄糖輸註率低于正常對照組(P<0.05),WIN55212-2組胰島素0~10 min分泌量、葡萄糖輸註率低于生理鹽水組(P<0.05).AM251組胰島素0~10 min分泌量、葡萄糖輸註率高于生理鹽水組和WIN55212-2組(P<0.05).結論 大痳素受體1受體激動可增加肥胖大鼠體質量,升高血脂水平,加重胰島素牴抗和胰島β細胞功能減退,抑製大痳素受體1可逆轉此效應.
목적 연구대마소수체1대비반대서이도β세포공능적영향.방법 30지8주령청길급건강웅성SD대서,체질최150~200 g,채용수자표법수궤분지정상대조조(n=6)화비반조(n=24).정상대조조급여보통서사료위양,비반조급여고지서사료위양.8주후,여정상대조조비교,비반뉴대서체질량증가36%,총담고순증가52%,제시24지비반대서제작성공.비반대서이수자표법수궤분지생리염수조(n=8)、WIN55212-2조(n=8)、AM251조(n=8).측정대서체질량、혈지、이도소、이도소원등지표,채용고포도당겸앙시험평개이도β세포공능화이도소민감성.채용LSD검험진행통계학분석.결과 복강주사약물2주후,생리염수조、WIN55212-2조체질량、혈지、졸복혈당、C태、이도소、이도소원、이도소원/C태、이도소원/이도소、이도소10~90 min분비량급이도소최대분비량균고우정상대조조(P<0.05),WIN55212-2조상술지표균고우생리염수조(P<0.05),AM251조상술지표균저우생리염수조화WIN55212-2조(P<0.05).생리염수조、WIN55212-2조이도소0~10 min분비량、포도당수주솔저우정상대조조(P<0.05),WIN55212-2조이도소0~10 min분비량、포도당수주솔저우생리염수조(P<0.05).AM251조이도소0~10 min분비량、포도당수주솔고우생리염수조화WIN55212-2조(P<0.05).결론 대마소수체1수체격동가증가비반대서체질량,승고혈지수평,가중이도소저항화이도β세포공능감퇴,억제대마소수체1가역전차효응.
Objective To investigate the effects of cannabinoind-1 receptor (CB1R) on pancreatic beta-cell function in obese rats. Methods A total of 30 male 8-week healthy SD rats were randomly assigned to the control group (n=6) or obesity group (n=24). After 8 weeks' intervention, 24 obese rats were randomly divided into the saline group (n=8), WIN55212-2 injection group (n=8) and AM251 injection group (n=8). The body weight, insulin, lipids, and proinsulin levels were measured in fasting status. Hyperglycemic clamp was performed to evaluate the insulin sensitivity and islet beta-cell function. LSD test was used for data analysis. Results After 2-week peritoneal injection, compared with the control group, body weight, lipids, fasting glucose, C peptide, insulin, proinsulin, proinsulin/C peptide, proinsulin/insulin, 10 to 90 min insulin release and maximum insulin secretion were significantly higher in the saline or WIN55212-2 injection group (all P <0.05). These parameters in the WIN55212-2 injection group were higher than those in the saline group (all P < 0.05). Above measurements in the AM251 injection group were lower than those in the saline or WIN55212-2 injection group (all P < 0.05). Compared with the control group, 0 to 10 min insulin release and glucose infusion rate (GIR) were significantly lower in the saline or WIN55212-2 injection group (all P < 0.05). GIR and 0 to 10 min insulin release in the WIN55212-2 injection group were lower than those in the saline group. GIR and 0 to 10 min insulin release in the AM251 injection group were higher than those in the saline or WIN55212-2 injection group. Conclusion Agitating CB1R could elevate body weight, lipid profile, insulin resistance and islet beta-cell function impairment in obese rats. Restraining CB1R could reverse those effectiveness.