Review: Placental programming of postnatal diabetes and impaired insulin action after IUGR.
Review: Placental programming of postnatal diabetes and impaired insulin action after IUGR.
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DOI：
10.1016/j.placenta.2009.12.015
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发表时间：
2010-03
期刊：
影响因子：
3.8
通讯作者：
Owens, J. A.
中科院分区：
文献类型：
--
作者：
Gatford, K. L.;Simmons, R. A.;De Blasio, M. J.;Robinson, J. S.;Owens, J. A.
由于出生前发育不良而出生时身材矮小，会增加日后患代谢疾病的风险，包括2型糖尿病。胰岛素分泌不足和胰岛素敏感性降低导致糖尿病风险增加。胎盘生长、发育和功能受损是胎儿生长发育受损并因此导致IUGR的主要原因。非人类动物胎盘生长（PR）和功能受限会引起与人类IUGR类似的胰岛素分泌和敏感性变化，使这些有价值的工具可用于研究潜在机制并测试干预措施以预防或改善IUGR后的疾病风险。由不良的胎儿环境引起的表观遗传变化强烈暗示是后来胰岛素作用受损的原因。这些已经在PR大鼠中得到了很好的表征，其中胰岛素分泌受损与Pdx-1启动子的表观遗传变化和该转录因子的表达减少有关。目前的研究特别集中在开发干预策略，以预防或逆转表观遗传变化，并使PR后的基因表达和胰岛素作用正常化，以便将其转化为改善人类IUGR结局的治疗方法。
Being born small due to poor growth before birth increases the risk of developing metabolic disease, including type 2 diabetes, in later life. Inadequate insulin secretion and decreasing insulin sensitivity contribute to this increased diabetes risk. Impaired placental growth, development and function are major causes of impaired fetal growth and development and therefore of IUGR. Restricted placental growth (PR) and function in non-human animals induces similar changes in insulin secretion and sensitivity as in human IUGR, making these valuable tools to investigate the underlying mechanisms and to test interventions to prevent or ameliorate the risk of disease after IUGR. Epigenetic changes induced by an adverse fetal environment are strongly implicated as causes of later impaired insulin action. These have been well-characterised in the PR rat, where impaired insulin secretion is linked to epigenetic changes at the Pdx-1 promotor and reduced expression of this transcription factor. Present research is particularly focussed on developing intervention strategies to prevent or reverse epigenetic changes, and normalise gene expression and insulin action after PR, in order to translate this to treatments to improve outcomes in human IUGR.
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