Acute food deprivation reduces expression of diazepam-binding inhibitor, the precursor of the anorexigenic octadecaneuropeptide ODN, in mouse glial cells
Acute food deprivation reduces expression of diazepam-binding inhibitor, the precursor of the anorexigenic octadecaneuropeptide ODN, in mouse glial cells
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DOI：
10.1677/jme-09-0176
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发表时间：
2010-05-01
影响因子：
3.5
通讯作者：
Tonon, M. C.
中科院分区：
文献类型：
--
作者：
Compere, V.;Lanfray, D.;Tonon, M. C.
在哺乳动物的中枢神经系统中，编码二氮卓结合抑制剂（DBI）的基因仅在神经胶质细胞中表达。先前的研究已经表明，DBI加工产品十八碳神经肽ODN的中央给药引起啮齿动物中食物消耗的显著抑制。然而，奇怪的是，食物限制对DBI基因表达的影响从未被研究过。在这里，我们表明，在小鼠中，急性禁食显着降低DBI mRNA水平在下丘脑和室管膜接壤的第三脑室和侧脑室。腹腔注射胰岛素，而不是瘦素，选择性刺激DBI表达在侧脑室区。这些数据支持的概念，神经胶质细胞，通过生产endozepines，可以中继外周信号的神经元参与中央调节能量稳态。
In the central nervous system of mammals, the gene encoding diazepam-binding inhibitor (DBI) is exclusively expressed in glial cells. Previous studies have shown that central administration of a DBI processing product, the octadecaneuropeptide ODN, causes a marked inhibition of food consumption in rodents. Paradoxically, however, the effect of food restriction on DBI gene expression has never been investigated. Here, we show that in mice, acute fasting dramatically reduces DBI mRNA levels in the hypothalamus and the ependyma bordering the third and lateral ventricles. I.p. injection of insulin, but not of leptin, selectively stimulated DBI expression in the lateral ventricle area. These data support the notion that glial cells, through the production of endozepines, may relay peripheral signals to neurons involved in the central regulation of energy homeostasis.