中华糖尿病杂志
中華糖尿病雜誌
중화당뇨병잡지
CHINES JOURNAL OF DLABETES MELLITUS
2013年
5期
301-305
,共5页
陈璐%唐暎%项守奎%华飞
陳璐%唐暎%項守奎%華飛
진로%당영%항수규%화비
胎儿生长迟缓%胰岛素合成相关基因%大鼠
胎兒生長遲緩%胰島素閤成相關基因%大鼠
태인생장지완%이도소합성상관기인%대서
Fetal growth retardation%Genes relevant to insulin synthesis%Rats
目的 研究宫内发育迟缓(IUGR)大鼠第36周胰腺组织中胰岛素合成相关基因表达的变化.方法 将20只体重250 ～ 270 g的8～ 10周健康雌性SD大鼠,饲养于无特定病原体(SPF)级动物房,适应性饲养2周后将雌雄鼠合笼,以发现阴栓当天记为雌鼠受孕第1天,雌鼠受孕后随机数字表法分为造模组(n=10)和对照组(n=10).采用孕中晚期热量限制的方法建立IUGR大鼠模型.造模组孕鼠自妊娠11d起给予对照组总热量50％饲料,新生鼠出生体重低于对照组新生鼠平均体重2个标准差者入选为IUGR组；对照组新生鼠即为正常组,对照组孕鼠自由进食.两组每窝各保留8只新生鼠继续饲养,仔鼠21 d断奶后以标准饲料喂养至36周.选取第36周(中老年阶段)雄鼠为研究对象,实施腹腔葡萄糖耐量及胰岛素释放试验,运用逆转录聚合酶链反应(RT-PCR)方法检测胰腺组织中胰岛素合成相关基因[胰岛素基因1(Insulin1)、胰岛素基因2(Insulin2)以及胰-十二指肠同源盒基因-1(PDX-1)]的表达情况.两组间比较采用t检验分析.结果 第36周,IUGR组大鼠胰重及胰重/体重比值明显低于正常组[分别为(4971±525)比(5844±398) mg和(0.58±0.05)％比(0.69±0.04)％,t=-2.65、-3.39,均P＜0.05].糖负荷后各时点(30、60、120、180 min)血糖值IUGR组均明显高于正常组[分别为30 min:(17.9±1.5)比(16.1±1.1) mmol/L,60 min:(13.4±1.1)比(11.7±1.4) mmol/L,120 min:(10.1 ±0.8)比(8.6±1.0) mmol/L,180 min:(8.9±1.0)比(7.6±0.9) mmol/L,=2.31、2.37、2.77、2.34,均P＜0.05]；糖负荷后各时点胰岛素分泌水平两组大鼠差异无统计学意义(t=1.66、-0.10、-0.65、-0.83、-0.58,均P＞0.05).IUGR组大鼠胰腺组织中Insulin1基因表达较正常组明显减少(0.79±0.17比1.25±0.28,t=-2.78,P＜0.05),而Insulin2、PDX-1基因表达差异均无统计学意义(t=-1.65、-1.46,均P＞0.05).结论 IUGR大鼠第36周糖耐量减退,胰腺组织中Insulin1基因表达下调.
目的 研究宮內髮育遲緩(IUGR)大鼠第36週胰腺組織中胰島素閤成相關基因錶達的變化.方法 將20隻體重250 ～ 270 g的8～ 10週健康雌性SD大鼠,飼養于無特定病原體(SPF)級動物房,適應性飼養2週後將雌雄鼠閤籠,以髮現陰栓噹天記為雌鼠受孕第1天,雌鼠受孕後隨機數字錶法分為造模組(n=10)和對照組(n=10).採用孕中晚期熱量限製的方法建立IUGR大鼠模型.造模組孕鼠自妊娠11d起給予對照組總熱量50％飼料,新生鼠齣生體重低于對照組新生鼠平均體重2箇標準差者入選為IUGR組；對照組新生鼠即為正常組,對照組孕鼠自由進食.兩組每窩各保留8隻新生鼠繼續飼養,仔鼠21 d斷奶後以標準飼料餵養至36週.選取第36週(中老年階段)雄鼠為研究對象,實施腹腔葡萄糖耐量及胰島素釋放試驗,運用逆轉錄聚閤酶鏈反應(RT-PCR)方法檢測胰腺組織中胰島素閤成相關基因[胰島素基因1(Insulin1)、胰島素基因2(Insulin2)以及胰-十二指腸同源盒基因-1(PDX-1)]的錶達情況.兩組間比較採用t檢驗分析.結果 第36週,IUGR組大鼠胰重及胰重/體重比值明顯低于正常組[分彆為(4971±525)比(5844±398) mg和(0.58±0.05)％比(0.69±0.04)％,t=-2.65、-3.39,均P＜0.05].糖負荷後各時點(30、60、120、180 min)血糖值IUGR組均明顯高于正常組[分彆為30 min:(17.9±1.5)比(16.1±1.1) mmol/L,60 min:(13.4±1.1)比(11.7±1.4) mmol/L,120 min:(10.1 ±0.8)比(8.6±1.0) mmol/L,180 min:(8.9±1.0)比(7.6±0.9) mmol/L,=2.31、2.37、2.77、2.34,均P＜0.05]；糖負荷後各時點胰島素分泌水平兩組大鼠差異無統計學意義(t=1.66、-0.10、-0.65、-0.83、-0.58,均P＞0.05).IUGR組大鼠胰腺組織中Insulin1基因錶達較正常組明顯減少(0.79±0.17比1.25±0.28,t=-2.78,P＜0.05),而Insulin2、PDX-1基因錶達差異均無統計學意義(t=-1.65、-1.46,均P＞0.05).結論 IUGR大鼠第36週糖耐量減退,胰腺組織中Insulin1基因錶達下調.
목적 연구궁내발육지완(IUGR)대서제36주이선조직중이도소합성상관기인표체적변화.방법 장20지체중250 ～ 270 g적8～ 10주건강자성SD대서,사양우무특정병원체(SPF)급동물방,괄응성사양2주후장자웅서합롱,이발현음전당천기위자서수잉제1천,자서수잉후수궤수자표법분위조모조(n=10)화대조조(n=10).채용잉중만기열량한제적방법건립IUGR대서모형.조모조잉서자임신11d기급여대조조총열량50％사료,신생서출생체중저우대조조신생서평균체중2개표준차자입선위IUGR조；대조조신생서즉위정상조,대조조잉서자유진식.량조매와각보류8지신생서계속사양,자서21 d단내후이표준사료위양지36주.선취제36주(중노년계단)웅서위연구대상,실시복강포도당내량급이도소석방시험,운용역전록취합매련반응(RT-PCR)방법검측이선조직중이도소합성상관기인[이도소기인1(Insulin1)、이도소기인2(Insulin2)이급이-십이지장동원합기인-1(PDX-1)]적표체정황.량조간비교채용t검험분석.결과 제36주,IUGR조대서이중급이중/체중비치명현저우정상조[분별위(4971±525)비(5844±398) mg화(0.58±0.05)％비(0.69±0.04)％,t=-2.65、-3.39,균P＜0.05].당부하후각시점(30、60、120、180 min)혈당치IUGR조균명현고우정상조[분별위30 min:(17.9±1.5)비(16.1±1.1) mmol/L,60 min:(13.4±1.1)비(11.7±1.4) mmol/L,120 min:(10.1 ±0.8)비(8.6±1.0) mmol/L,180 min:(8.9±1.0)비(7.6±0.9) mmol/L,=2.31、2.37、2.77、2.34,균P＜0.05]；당부하후각시점이도소분비수평량조대서차이무통계학의의(t=1.66、-0.10、-0.65、-0.83、-0.58,균P＞0.05).IUGR조대서이선조직중Insulin1기인표체교정상조명현감소(0.79±0.17비1.25±0.28,t=-2.78,P＜0.05),이Insulin2、PDX-1기인표체차이균무통계학의의(t=-1.65、-1.46,균P＞0.05).결론 IUGR대서제36주당내량감퇴,이선조직중Insulin1기인표체하조.
Objective To investigate the expression of genes relevant to insulin synthesis of intrauterine growth retardation(IUGR) rats at 36 weeks.Methods Twenty healthy female SD rats (250-270 g; 8-10 weeks old) were housed in the SPF animal room.After two weeks acclimatization,male and female rats were placed in same cage overnight for mating.Day 1 of pregnancy was defined as the day on which vaginal plugs were found.Female rats were grouped into normal controls (n =10) and model group (n =10) according to random number table.The IUGR rat model was established by maternal nutrition restriction during mid-to late-gestation.Pregnant rats received 50％ of their daily food intake beginning from day 11 through day 21 of gestation,compared with their control counterparts who had free access to rat chow.The birth weights of the offsprings born to semistarvation mothers were more than two times of standard deviation below the mean values of the birth weights of the control group with IUGR.The litter size was randomly reduced to eight at birth to assure uniformity of litter size between IUGR and control litters.Two groups of pups were fostered to their mothers until they were weaned at day 21,and then all the pups were fed with standard rat chow until 36 weeks of life.Male offsprings at 36 weeks of age were selected asresearch subjects.Intraperitoneal glucose tolerance test (IPGTT) and insulin releasing test (IRT) were performed in IUGR and normal groups.RT-PCR was applied to detect the expression of pancreas genes such as Insulin1,Insulin2 and PDX-1.The t test was used in the comparison between two groups.Results At 36 weeks of age,body weight,pancreas weight and pancreas/body weight in IUGR group were much lower than those in normal group ((4971 ±525) and (5844 ±398) mg,(0.58 ±0.05)％ and (0.69 ±0.04)％respectively,t =-2.65 and-3.39,both P ＜ 0.05).Glucose levels at 30,60,120 and 180 min after glucose load were significantly higher in IUGR group (30 min:(17.9 ± 1.5) vs (16.1 ± 1.1) mmol/L,60min:(13.4±1.1) vs(11.7±1.4) mmol/L,120min:(10.1±0.8) vs (8.6±1.0) mmol/L,180min:(8.9±1.0) vs (7.6±0.9) mmol/L,t =2.31,2.37,2.77,2.34,all P＜0.05),indicated glucose tolerance was impaired in IUGR rats.In addition,there was no significant difference in the insulin levels at the time points during glucose tolerance test between normal and IUGR rats (t =1.66,-0.10,-0.65,-0.83,-0.58,P ＞0.05).In IUGR rats,the expressions of Insulin1 mRNA were reduced markedly than those in the controls (0.79 ± 0.17 vs 1.25 ± 0.28,t =-2.78,P ＜ 0.05).Although no significant differences were observed in gene expression of Insulin2 mRNA and PDX-1 mRNA (both P ＞ 0.05).Conclusions The IUGR rats had deteriorated glucose tolerance at 36 weeks of age with decreased gene expression of Insulin1 in pancreas.
