首页> 外文期刊>Life sciences >Diabetic pregnancy in rats leads to impaired glucose metabolism in offspring involving tissue-specific dysregulation of 11beta-hydroxysteroid dehydrogenase type 1 expression.
【24h】

Diabetic pregnancy in rats leads to impaired glucose metabolism in offspring involving tissue-specific dysregulation of 11beta-hydroxysteroid dehydrogenase type 1 expression.

机译:大鼠糖尿病妊娠导致后代的葡萄糖代谢受损,涉及11β-羟类固醇脱氢酶1型表达的组织特异性失调。

获取原文
获取原文并翻译 | 示例
           

摘要

Population-based studies have shown that the offspring of diabetic mothers have an increased risk of developing obesity, insulin resistance, type 2 diabetes and hypertension in later life. To investigate mechanism for the high incidence of metabolic diseases in the offspring of diabetic mothers, we focused on the tissue-specific glucocorticoid regulation by 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) and studied offspring born to streptozotocin-induced diabetic rats. The body weights of newborn rats from diabetic mothers were heavier than those from control mothers. Offspring born to diabetic mothers demonstrated insulin resistance and mild glucose intolerance after glucose loading at 10 weeks and showed significantly increased 11beta-HSD1 mRNA and enzyme activity in adipose tissue at 12 weeks of age without obvious obesity. Hepatic 11beta-HSD1 mRNA was also elevated. We propose that the 11beta-HSD1 in adipose tissue and liver may play a key role in the development of metabolic syndrome inthe offspring of diabetic mothers. Tissue-specific glucocorticoid dysregulation provides a candidate mechanism for the high incidence of metabolic diseases in the offspring of diabetic mothers. Therefore early analyses before apparent obesity are needed to elucidate the molecular mechanisms that may be programmed during the fetal period.
机译:基于人群的研究表明,糖尿病母亲的后代在以后的生活中患肥胖症,胰岛素抵抗,2型糖尿病和高血压的风险增加。为了研究糖尿病母亲后代中代谢疾病高发的机制,我们集中于11β-羟类固醇脱氢酶1型(11β-HSD1)对组织特异性糖皮质激素的调控,并研究了链脲佐菌素诱导的糖尿病大鼠的后代。糖尿病母亲的新生大鼠体重比对照组母亲的体重重。糖尿病母亲的后代在10周的葡萄糖负荷后表现出胰岛素抵抗和轻度的葡萄糖耐受不良,并且在12周龄的脂肪组织中显示11beta-HSD1 mRNA和酶活性显着增加,而没有明显的肥胖。肝11beta HSD1 mRNA也升高。我们建议,在脂肪组织和肝脏中的11beta-HSD1可能在糖尿病母亲的后代代谢综合征的发展中起关键作用。组织特异性糖皮质激素失调为糖尿病母亲的后代中代谢疾病的高发病率提供了候选机制。因此,需要在出现明显肥胖之前进行早期分析,以阐明胎儿期可能编程的分子机制。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号