Programming of hypothalamic functions regulating energy homeostasis may play a role in intrauterine growth restriction (IUGR)-induced adulthood obesity. The present study investigated the effects of IUGR on the hypothalamus proteome and metabolome of adult rats submitted to 50% protein-energy restriction throughout pregnancy. Proteomic and metabolomic analyzes were performed by data independent acquisition mass spectrometry and multiple reaction monitoring, respectively. At age 4 months, the restricted rats showed elevated adiposity, increased leptin and signs of insulin resistance. 1356 proteins were identified and 348 quantified while 127 metabolites were quantified. The restricted hypothalamus showed down-regulation of 36 proteins and 5 metabolites and up-regulation of 21 proteins and 9 metabolites. Integrated pathway analysis of the proteomics and metabolomics data indicated impairment of hypothalamic glucose metabolism, increased flux through the hexosamine pathway, deregulation of TCA cycle and the respiratory chain, and alterations in glutathione metabolism. The data suggest IUGR modulation of energy metabolism and redox homeostasis in the hypothalamus of male adult rats. The present results indicated deleterious consequences of IUGR on hypothalamic pathways involved in pivotal physiological functions. These results provide guidance for future mechanistic studies assessing the role of intrauterine malnutrition in the development of metabolic diseases later in life.

译文

调节能量稳态的下丘脑功能的编程可能在宫内生长受限 (IUGR) 引起的成年期肥胖中起作用。本研究调查了IUGR对整个怀孕期间50% 蛋白质能量限制的成年大鼠的下丘脑蛋白质组和代谢组的影响。蛋白质组学和代谢组学分析分别通过数据独立采集质谱和多反应监测进行。在4个月大时,限制性大鼠表现出肥胖升高,瘦素增加和胰岛素抵抗的迹象。鉴定1356蛋白质并348定量,同时定量127代谢物。受限制的下丘脑显示出36种蛋白质和5种代谢产物的下调,而21种蛋白质和9种代谢产物的上调。蛋白质组学和代谢组学数据的综合途径分析表明,下丘脑葡萄糖代谢受损,通过己糖胺途径的通量增加,TCA循环和呼吸链的失调以及谷胱甘肽代谢的改变。数据表明IUGR调节了雄性成年大鼠下丘脑的能量代谢和氧化还原稳态。目前的结果表明,IUGR对涉及关键生理功能的下丘脑途径的有害影响。这些结果为将来评估子宫内营养不良在以后生活中代谢疾病发展中的作用的机制研究提供了指导。

+1
+2
100研值 100研值 ¥99课程
检索文献一次
下载文献一次

去下载>

成功解锁2个技能,为你点赞

《SCI写作十大必备语法》
解决你的SCI语法难题!

技能熟练度+1

视频课《玩转文献检索》
让你成为检索达人!

恭喜完成新手挑战

手机微信扫一扫,添加好友领取

免费领《Endnote文献管理工具+教程》

微信扫码, 免费领取

手机登录

获取验证码
登录