中华糖尿病杂志
中華糖尿病雜誌
중화당뇨병잡지
CHINES JOURNAL OF DLABETES MELLITUS
2011年
6期
478-481
,共4页
张明亮%朱云霞%尹德超%李羚%陆俊茜%王琛%贾伟平
張明亮%硃雲霞%尹德超%李羚%陸俊茜%王琛%賈偉平
장명량%주운하%윤덕초%리령%륙준천%왕침%가위평
糖尿病%小鼠%高葡萄糖钳夹技术%胰岛β细胞
糖尿病%小鼠%高葡萄糖鉗夾技術%胰島β細胞
당뇨병%소서%고포도당겸협기술%이도β세포
Diabetes mellitus%Mice%Hyperglycemic clamp technique%Pancreatic β cell
目的 利用高葡萄糖钳夹技术探讨高糖喂养小鼠胰岛β细胞功能.方法 将16只4周龄C57BL/6J品系小鼠随机数字表法分为2组(各8只),分别用高糖与普通饲料喂养,8周后行腹腔葡萄精耐量实验比较2组小鼠葡萄糖耐量,行胰岛素耐量实验比较2组小鼠外周组织对胰岛素的敏感性,应用高葡萄糖钳夹技术比较模型小鼠在体胰岛β细胞第1时相和第2时相胰岛素分泌改变.钳夹实验结束3~4d后麻醉动物,取小鼠肝脏,利用庚烷-异丙醇-吐温的方法提取肝脏内甘油三酯及总胆固醇.组间数据比较采用t检验.结果 喂养10周时,高糖组小鼠体质量[(18.o±0.8)g]低于普食组[(23.6±0.5)g],2组差异有统计学意义(t=5.595,P<0.05).高糖组糖耐昔曲线下面积为( 103±3)mmol/L,显著高于普食组的(91±3)mmol/L(t=2.487,P<0.05).普食组葡萄糖利用指数(KITT)与高糖组差异无统计学意义(分别为0.53±0.08和0.54±0.14,t=2.360,P>0.05).高葡萄糖钳夹显示,高糖组第1时相胰岛素水平较普食组下降了49.6%[分别为(0.71±0.26)和(1.41±0.44) μg/L; =2.943,P<0.05];高糖组平均葡萄糖输注率为(6.8 ±2.2)mg· kg-1·min-1,也较普食组的(20.2±2.3)mg· kg-1·min-1降低了66.3%(t=4.206,P<0.05).结论 高糖喂养早期(8周),小鼠发生葡萄糖耐量降低,主要为胰岛β细胞第1时相胰岛素分泌减弱所致,并非外周胰岛素敏感性改变引起.
目的 利用高葡萄糖鉗夾技術探討高糖餵養小鼠胰島β細胞功能.方法 將16隻4週齡C57BL/6J品繫小鼠隨機數字錶法分為2組(各8隻),分彆用高糖與普通飼料餵養,8週後行腹腔葡萄精耐量實驗比較2組小鼠葡萄糖耐量,行胰島素耐量實驗比較2組小鼠外週組織對胰島素的敏感性,應用高葡萄糖鉗夾技術比較模型小鼠在體胰島β細胞第1時相和第2時相胰島素分泌改變.鉗夾實驗結束3~4d後痳醉動物,取小鼠肝髒,利用庚烷-異丙醇-吐溫的方法提取肝髒內甘油三酯及總膽固醇.組間數據比較採用t檢驗.結果 餵養10週時,高糖組小鼠體質量[(18.o±0.8)g]低于普食組[(23.6±0.5)g],2組差異有統計學意義(t=5.595,P<0.05).高糖組糖耐昔麯線下麵積為( 103±3)mmol/L,顯著高于普食組的(91±3)mmol/L(t=2.487,P<0.05).普食組葡萄糖利用指數(KITT)與高糖組差異無統計學意義(分彆為0.53±0.08和0.54±0.14,t=2.360,P>0.05).高葡萄糖鉗夾顯示,高糖組第1時相胰島素水平較普食組下降瞭49.6%[分彆為(0.71±0.26)和(1.41±0.44) μg/L; =2.943,P<0.05];高糖組平均葡萄糖輸註率為(6.8 ±2.2)mg· kg-1·min-1,也較普食組的(20.2±2.3)mg· kg-1·min-1降低瞭66.3%(t=4.206,P<0.05).結論 高糖餵養早期(8週),小鼠髮生葡萄糖耐量降低,主要為胰島β細胞第1時相胰島素分泌減弱所緻,併非外週胰島素敏感性改變引起.
목적 이용고포도당겸협기술탐토고당위양소서이도β세포공능.방법 장16지4주령C57BL/6J품계소서수궤수자표법분위2조(각8지),분별용고당여보통사료위양,8주후행복강포도정내량실험비교2조소서포도당내량,행이도소내량실험비교2조소서외주조직대이도소적민감성,응용고포도당겸협기술비교모형소서재체이도β세포제1시상화제2시상이도소분비개변.겸협실험결속3~4d후마취동물,취소서간장,이용경완-이병순-토온적방법제취간장내감유삼지급총담고순.조간수거비교채용t검험.결과 위양10주시,고당조소서체질량[(18.o±0.8)g]저우보식조[(23.6±0.5)g],2조차이유통계학의의(t=5.595,P<0.05).고당조당내석곡선하면적위( 103±3)mmol/L,현저고우보식조적(91±3)mmol/L(t=2.487,P<0.05).보식조포도당이용지수(KITT)여고당조차이무통계학의의(분별위0.53±0.08화0.54±0.14,t=2.360,P>0.05).고포도당겸협현시,고당조제1시상이도소수평교보식조하강료49.6%[분별위(0.71±0.26)화(1.41±0.44) μg/L; =2.943,P<0.05];고당조평균포도당수주솔위(6.8 ±2.2)mg· kg-1·min-1,야교보식조적(20.2±2.3)mg· kg-1·min-1강저료66.3%(t=4.206,P<0.05).결론 고당위양조기(8주),소서발생포도당내량강저,주요위이도β세포제1시상이도소분비감약소치,병비외주이도소민감성개변인기.
Objective To evaluate the pancreatic β cell function in sucrose-fed mice by hyperglycemic clamp technique.Methods Sixteen C57BL/6J mice were randomly divided into two groups and fed with either high sucrose diet ( n =8 ) or chow food ( n =8 ) for 8 weeks.Intraperitoneal glucose tolerance test (IPGTT) was carried out to detect glucose tolerance,intraperitoneal insulin tolerance test was applied to detect peripheral insulin sensitivity,hyperglycemic clamp technique was used to detect the first and second phase of insulin secretion in the two groups.Liver lipids were extracted with heptane-isopropanoltween methods in the mice.The data was compared between the two groups by using t test.Results In contrast to chow-fed mice,the body weight of sucrose-fed mice decreased by 23.4 % ( ( 23.6 ± 0.5 ) g and ( 18.0 ± 0.8 ) g,respectively; t =5.595,P < 0.001 ).The area under the IPGTT curve from sucrose-fed mice was much higher than that from chow-fed mice (( 103 ± 3 ) mmol/L and (91 ± 3 ) mmol/L,respectively; t =2.487,P < 0.05 ).No difference could be observed in glucose disappearance rate (KITT) between the two groups ( 0.53 ± 0.08 and 0.54 ± 0.14,respectively ; t =2.360,P > 0.05 ).During hyperglycemic clamp,the first phase of insulin secretion decreased by 49.6% in sucrose-fed mice compared with that in chow-fed mice ((0.71 ±0.26) μg/L and (1.41 ±0.44) μg/L,respectively; t =2.943,P< 0.05 ).The average glucose infusion rate (GIR) was ( 20.2 ± 2.3 ) mg · kg- 1 · min - 1 in chow-fed mice and which was decreased by 66.3 % in sucrose-fed mice ( (6.8 ± 2.2) mg · kg- 1 · min- 1 ) ( t =4.206,P < 0.05) from the sucrose-fed mice.Conclusions Eight-week feeding with a high sucrose diet in mice induced glucose intolerance.It might be due to reduction in the first phase insulin secretion from pancreatic β cells,but not to peripheral insulin resistance.