首页> 外文学位 >Maternal docosahexanoic acid supplementation increases adiponectin expression in intrauterine growth restricted rats.
【24h】

Maternal docosahexanoic acid supplementation increases adiponectin expression in intrauterine growth restricted rats.

机译:母体二十二碳六烯酸的补充可增加宫内生长受限大鼠的脂联素表达。

获取原文
获取原文并翻译 | 示例

摘要

Intrauterine growth restriction (IUGR) increases the risk of obesity and insulin resistance in adulthood. Insulin resistance is inversely correlated with serum adiponectin levels. Adiponectin expression increases with PPARgamma activation by docosahexanoic acid (DHA). We have previously shown that IUGR results in PPARgamma dysregulation in adipose tissue before the onset of obesity and that its expression can be normalized by maternal DHA administration.;However, the effect of IUGR and PPARgamma activation on adiponectin production in the rat is unknown. We hypothesize that adding DHA to the maternal diet will increase subcutaneous adipose tissue (SAT) adiponectin and adiponectin receptor mRNA and protein and serum adiponectin.;IUGR was induced by bilateral uterine artery ligation at E19 of gestation. Maternal rats were fed a standard diet or a 1% DHA diet from E13 to term and during lactation. The effect of IUGR on mRNA levels of adiponectin and its receptors (AdipoR1 and AdipoR2) in SAT and visceral adipose tissue (VAT) of d21 rats was measured by real-time RT-PCR. Serum adiponectin levels were measured by ELISA. Protein levels were measure by western blotting.;In regular diet rats, IUGR significantly increased mRNA levels of AdipoR1 in VAT and AdipoR2 in SAT of males. DHA supplementation on IUGR significantly increased mRNA levels of adiponectin (236+/-16%*), AdipoR1 (189+/-15%*), and Adipor2 (384+/- 65%*) in male SAT and adiponectin (199+/-16%*) and AdipoR2 (425+/-23%*) in female SAT. AdipoR1 and R2 protein levels were increased in male (220+/-38%; 255+/-51%*) and female (202+/-19%*; 229+/-22%) SAT. Serum adiponectin levels were increased in males (149+/-13%*) and females (156+/-11%*) *p0.05.;We conclude that IUGR results in an altered expression of adiponectin and its receptors. Maternal DHA supplementation increases SAT adiponectin, AdipoR1/2 mRNA and protein, and serum adiponectin levels in IUGR rats. We speculate that increased adiponectin production in DHA supplemented IUGR rats may protect against the development of insulin resistance in adulthood.
机译:宫内生长受限(IUGR)增加了成年后肥胖和胰岛素抵抗的风险。胰岛素抵抗与血清脂联素水平成反比。脂联素的表达随着二十二碳六烯酸(DHA)激活PPARγ而增加。先前我们已经证明IUGR会在肥胖发作之前导致脂肪组织中的PPARγ失调,并且其表达可以通过母体DHA给药来标准化。我们假设在母体饮食中添加DHA会增加皮下脂肪组织(SAT)脂联素和脂联素受体mRNA和蛋白以及血清脂联素的含量。IUGR是在妊娠E19时经双侧子宫动脉结扎诱导的。从E13到足月和哺乳期间,给母鼠喂食标准饮食或1%DHA饮食。通过实时RT-PCR测量IUGR对d21大鼠SAT和内脏脂肪组织(VAT)中脂联素及其受体(AdipoR1和AdipoR2)mRNA水平的影响。通过ELISA测量血清脂联素水平。通过蛋白质印迹法测量蛋白质水平。在常规饮食大鼠中,IUGR显着增加了雄性动物的VAT中AdipoR1和SAT中的AdipoR2 mRNA水平。在IUGR上添加DHA显着增加了男性SAT和脂联素(199+)中脂联素(236 +/- 16%*),AdipoR1(189 +/- 15%*)和Adipor2(384 +/- 65%*)的mRNA水平。 / -16%*)和女性SAT中的AdipoR2(425 +/- 23%*)。男性(220 +/- 38%; 255 +/- 51%*)和女性(202 +/- 19%*; 229 +/- 22%)SAT的AdipoR1和R2蛋白水平升高。男性(149 +/- 13%*)和女性(156 +/- 11%*)的血清脂联素水平增加* p <0.05。我们得出的结论是,IUGR导致脂联素及其受体表达的改变。母体DHA补充可增加IUGR大鼠的SAT脂联素,AdipoR1 / 2 mRNA和蛋白质以及血清脂联素水平。我们推测,在补充DHA的IUGR大鼠中增加脂联素的产生可能防止成年期胰岛素抵抗的发展。

著录项

  • 作者

    Bagley, Heidi.;

  • 作者单位

    The University of Utah.;

  • 授予单位 The University of Utah.;
  • 学科 Health Sciences Nutrition.
  • 学位 M.S.
  • 年度 2010
  • 页码 32 p.
  • 总页数 32
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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