Dietary vitamin and lipid therapy rescues aberrant signaling and apoptosis and prevents hyperglycemia-induced diabetic embryopathy in rats
Dietary vitamin and lipid therapy rescues aberrant signaling and apoptosis and prevents hyperglycemia-induced diabetic embryopathy in rats
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DOI：
10.1016/j.ajog.2005.08.052
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发表时间：
2006-02-01
影响因子：
9.8
通讯作者：
Dhanasekaran, D
中科院分区：
文献类型：
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作者：
Reece, EA;Wu, YK;Dhanasekaran, D
目的：母体糖尿病导致胚胎发育畸形。膳食中补充抗氧化剂可以降低动物模型的畸形率。为了研究糖尿病诱导的胚胎异常和饮食干预的分子机制，丝裂原活化蛋白激酶的活性和与凋亡途径相关的因子在母体糖尿病大鼠model.Study设计：糖尿病诱导妊娠大鼠使用链脲佐菌素。在胚胎的卵黄囊中，细胞外信号调节激酶Raf-1和Akt的活性在糖尿病大鼠中显著降低，而c-jun N-末端激酶/应激活化蛋白激酶的活性增加。当糖尿病母鼠喂食花生四烯酸、维生素E或花生四烯酸、维生素E和肌醇的组合时，这些激酶表达的改变被逆转，并与凋亡率和胚胎畸形率的降低相关。这些结果表明，丝裂原活化蛋白激酶参与糖尿病胚胎病，饮食干预可以挽救异常的信号通路，降低胚胎畸形率。(c)2006 Mosby，Inc. All rights reserved.
Objective: Maternal diabetes causes developmental malformations in the embryo. Dietary supplementation with antioxidants can reduce the malformation rates in animal models. To investigate the molecular mechanisms underlying diabetes-induced embryonic abnormalities and dietary interventions, activity of mitogen-activated protein kinases and factors associated with apoptotic pathways were examined in the maternal diabetic rat model.Study design: Diabetes was induced in pregnant rats using streptozotocin. In the yolk sacs of the embryos, activity of the extracellular signal-regulated kinases, Raf-1, and Akt was dramatically reduced in diabetic rats, whereas that of c-jun N-terminal kinases/stress-activated protein kinases was increased.Results: When the diabetic dams were fed with arachidonic acid, vitamin E, or a combination of arachidonic acid, vitamin E, and myoinositol, the changes in the expression of these kinases were reversed and correlated with the decreases in the rates of apoptosis and embryonic malformations.Conclusion: These results suggest that mitogen-activated protein kinases are involved in diabetic embryopathy, and dietary supplementations can rescue the aberrant signaling pathways and reduce embryonic malformation rate. (c) 2006 Mosby, Inc. All rights reserved.