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首页> 外文期刊>Life sciences >Carbaprostacyclin, a PPARdelta agonist, ameliorates excess lipid accumulation in diabetic rat placentas.
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Carbaprostacyclin, a PPARdelta agonist, ameliorates excess lipid accumulation in diabetic rat placentas.

机译：PPARδ激动剂Carbaprostacyclin可改善糖尿病大鼠胎盘中过多的脂质蓄积。

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摘要

AIMS: Maternal diabetes impairs placental development and metabolism. Peroxisome proliferator-activated receptors (PPARs) are ligand-activated nuclear receptors relevant in metabolic homeostasis. We investigated the concentrations of PPARdelta and its endogenous agonist prostacyclin (PGI2), as well as the effects of carbaprostacylin (cPGI(2,) a PPARdelta agonist) on lipid metabolism in placentas from control and streptozotocin-induced diabetic rats on day 13.5 of gestation. MAIN METHODS: The placentas were explanted to evaluate PPARdelta expression and PGI2 concentrations, and cultured with cPGI2 for further analysis of lipid metabolism (concentrations and (14)C-acetate derived synthesis of triglycerides, cholesteryl esters, phospholipids, cholesterol and free fatty acids; release of glycerol and lipid peroxidation). KEY FINDINGS: Reduced PGI2 concentrations were found in the placentas from diabetic rats when compared to controls. cPGI2 additions reduced the concentrations and synthesis of several lipid species, increased lipid catabolism and reduced lipid peroxidation in the placenta. These effects were more marked in diabetic tissues, which presented alterations in the lipid metabolic parameters evaluated. cPGI2 additions increased placental PPARdelta and acyl-CoA oxidase expression, which are changes possibly involved in the catabolic effects observed. SIGNIFICANCE: The present study reveals the capability of cPGI2 to regulate placental lipid metabolism and PPARdelta expression, and suggests that preserving appropriate PGI2 concentrations in the placenta may help to metabolize maternal derived lipid overload in diabetic gestations.
机译：目的：母体糖尿病会损害胎盘发育和新陈代谢。过氧化物酶体增殖物激活受体（PPAR）是与代谢稳态相关的配体激活核受体。我们在妊娠第13.5天调查了对照和链脲佐菌素诱导的糖尿病大鼠胎盘中PPARδ及其内源性激动剂前列环素（PGI2）的浓度，以及碳前列环素（cPGI（2，）PPARδ激动剂）对胎盘脂质代谢的影响。 。主要方法：植入胎盘以评估PPARδ的表达和PGI2的浓度，并与cPGI2培养以进一步分析脂质代谢（浓度和（14）C-乙酸酯合成的甘油三酸酯，胆固醇酯，磷脂，胆固醇和游离脂肪酸;释放甘油和脂质过氧化）。主要发现：与对照组相比，发现糖尿病大鼠胎盘中PGI2浓度降低。 cPGI2的添加降低了几种脂质种类的浓度和合成，增加了脂质分解代谢并减少了胎盘中脂质的过氧化作用。这些作用在糖尿病组织中更为明显，这表明所评估的脂质代谢参数发生了变化。添加cPGI2会增加胎盘PPARδ和酰基CoA氧化酶的表达，这可能与观察到的分解代谢作用有关。重要性：本研究揭示了cPGI2调节胎盘脂质代谢和PPARdelta表达的能力，并表明在胎盘中保留适当的PGI2浓度可能有助于代谢母体衍生的糖尿病性脂质超负荷。

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