Regulation of apelin mRNA expression by insulin and glucocorticoids in mouse 3T3-L1 adipocytes

Regulation of apelin mRNA expression by insulin and glucocorticoids in mouse 3T3-L1 adipocytes
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DOI:
10.1016/j.regpep.2005.08.003
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发表时间:
2005-12-15
影响因子:
--
通讯作者:
Tatemoto, K
Tatemoto, K
中科院分区:
其他
文献类型:
--
作者:
Wei, L;Hou, XH;Tatemoto, K

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新的36个氨基酸的肽,apelin,是孤儿受体APJ的内源性配体。Apelin可能在心血管系统和下丘脑-垂体轴的调节中起重要作用。它是一种有效的降压剂,也是最有效的心脏收缩刺激剂之一。在这项研究中,我们研究了来自脂肪细胞的apelin在调节心血管稳态中的作用。我们发现apelin和APJ mRNA在小鼠离体脂肪细胞中均有表达,并且在3T3-L1细胞向脂肪细胞分化的过程中apelin mRNA水平升高。我们还发现胰岛素(1 nM-100 nM)增加,而地塞米松(0.1 nM-100 nM)以剂量依赖的方式降低3T3-L1脂肪细胞中apelin mRNA水平,表明胰岛素和糖皮质激素调节脂肪细胞中apelin基因表达。我们推测,高糖皮质激素水平抑制了脂肪细胞中apelin的产生并刺激了血管紧张素II的产生,从而降低了apelin对血管紧张素II升压作用的反调节活性,这可能在一定程度上参与了肥胖相关性高血压发生的机制。(c) 2005 Elsevier B.V.版权所有
The novel 36-amino acid peptide, apelin, is the endogenous ligand for the orphan receptor APJ. Apelin may play important roles in the regulation of the cardiovascular system and the hypothalamic-pituitary axis. It is a potent hypotensive agent and one of the most potent stimulators of cardiac contractility. In this study, we investigated the roles of apelin derived from adipocytes in the regulation of cardiovascular homeostasis. We found that both apelin and APJ mRNAs were expressed in isolated mouse adipocytes and that apelin mRNA levels increased during the differentiation of 3T3-L1 cells to adipocytes. We also found that the administration of insulin (1 nM-100 nM) increased, while that of dexamethasone (0.1 nM-100 nM) decreased the apelin mRNA levels in 3T3-L1 adipocytes in a dose-dependent manner, suggesting that insulin and glucocorticoids regulate apelin gene expression in adipocytes. We speculate that high glucocorticoid levels suppress apelin production and stimulate angiotensin II production in adipocyte, decreasing the counter-regulatory activity of apelin against the pressor action of angiotensin II, which might partly be involved in the mechanism underlying the development of obesity-related hypertension. (c) 2005 Elsevier B.V. All rights reserved.