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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 study the expression of PDX-1, a key factor in pancreatic development and differentiation of intrauterine growth-restricted (IUGR) rats, and to investigate the effects of IUGR on pancreatic β-cell development The molecular mechanism of impairment and dysfunction. Methods To establish a rat model of intrauterine growth restriction. In the low-protein diet group, the female rats were given the same caloric low protein feed from the first day after conception till the delivery; the control group was fed with normal feed. After natural childbirth, weighed the weight of newborn offspring, measured the length of the nose and tail, removed the pancreas, and examined the expression of PDX-1 in the pancreas of neonatal rats by immunohistochemical staining. Results (1) The birth weight, length of nasal tail, and weight of pancreas in IU-GR neonatal rats were lower than those in control group (P <0.01). (2) The expression of PDX-1 in the pancreas of IUGR newborn rats was significantly lower than that of the control group (P <0.01). Conclusions Intrauterine protein malnutrition induced IUGR. At the time point of newborn rats, the weight of pancreas was significantly lower than that of the control group. The expression of PDX-1 in the pancreas decreased especially significantly, which was twice as much as that of the weight loss (48%: 23 %), Which is a multiple of 5.5 (48%: 8.6%) decrease in pancreatic weight. The decrease in PDX-1 may be one of the molecular mechanisms that cause the development of pancreas and / or pancreatic β-cell dysfunction.