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作 者:刘颖[1] 张雅静[1] 付大军[1] 程士凯[1] 成晓君[1] 李书琴[2]
机构地区:[1]中国医科大学附属第四医院儿科,沈阳110033 [2]中国医科大学附属盛京医院实验研究中心
出 处:《中国优生与遗传杂志》2011年第6期27-28,87,共3页Chinese Journal of Birth Health & Heredity
摘 要:目的研究宫内营养不良致宫内生长受限(IUGR)大鼠胰腺发育、分化的关键因子胰十二指肠同源盒1(PDX-1)的表达,探讨IUGR个体胰腺中β细胞发育受损及机能障碍的分子学机制。方法建立宫内生长受限大鼠模型。低蛋白饮食组,雌性大鼠自受孕后第1天起给予同热卡低蛋白饲料喂养直至分娩;对照组给予普通饲料喂养。自然分娩后,称取新生仔鼠体重,测量鼻尾长,摘取胰腺,免疫组织化学染色方法检测新生大鼠胰腺中PDX-1的表达。结果 (1)IU-GR新生大鼠出生体重、鼻尾长及胰腺重量均低于对照组(P<0.01)。(2)IUGR新生大鼠胰腺中PDX-1的表达明显低于对照组(P<0.01)。结论宫内蛋白营养不良大鼠致IUGR,在新生鼠时间点,胰腺重量明显低于对照组,胰腺中PDX-1表达下降尤其严重,其下降幅度为体重减轻幅度的2倍(48%:23%),为胰腺重量降低的5.5(48%:8.6%)倍之多,PDX-1降低可能是造成胰腺发育落后和/或胰岛β细胞功能障碍的分子机制之一。Objective:To explore the molecular mechanism of impaired development and functional maturation of β-cell in intrauterine growth restriction(IUGR),and to detect the effects of malnutrition in uterine on the expression of pancreatic and duodenal homeobox 1(PDX-1)in pancreatic islets.Methods: The dams were administrated with an isoenergetic diet containing low protein from the first day during pregnancy to build the animal model of IUGR,while the control group with normal protein.After spontaneous delivery of the dams,the newborn rats' body weight and the lenth of nose-tail were measured,and the pancreas of the newborn rats were weighted.Immunohistochemistry staining was conducted to analyze the expression of PDX-1.Results:(1) The weight,lenth of nose-tail and pancreatic islets weight were markedly depressed in IUGR group compared with the control group(P0.01).(2) The expression of PDX-1 was significantly lower in pancreatic islets of IUGR group than that in control(P0.01).Conclusion: For protein malnutrition in urterine induced IUGR,at birth of the rats,the pancreatic weight were obviously lower than that of control.The PDX-1 expression in pancreatic islets decreased even more,whose decrease proportion was two times of that of body weight(48%,23%),and five and a half times of that of pancreatic weight(48%,8.6%).Thus,the decline of PDX-1 might be one of the molecular mechanisms of pancreatic development lag and β-cell dysfunction.IUGR
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