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首页> 外文会议>Conference on Brain Somatic Cross Talk and the Central Control of Metabolism >Interactions of Growth Hormone Secretagogues With Leptin-sensitive Brain Networks
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Interactions of Growth Hormone Secretagogues With Leptin-sensitive Brain Networks

机译：生长激素分泌术与瘦素敏感脑网络的相互作用

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The growth hormone secretagogues (GHS) and ghrelin, an endogenous ligand for the cloned GHS receptor, have recently been shown to induce adiposity in rodents. For some time now, we have been investigating the central site and mechanism of action of GHS, mostly in relation to their growth hormone-releasing action. However, it has become clear that these compounds can activate neuropep-tide Y-containing neurones and interact with the hypothalamic circuits controlling body weight and appetite. GHS and ghrelin induce adiposity, although the CNS mechanism underlying this effect may not be fully understood. Hypothalamic circuits regulating body weight can be readily identified as they are responsive to circulating satiety factors such as leptin and insulin. Thus, in electrophysi-ological studies in vitro we have shown that cells excited by GHS tend to be inhibited by leptin administration. Moreover, GHS-responsive cells appear to be direct targets for leptin, as these responses to GHS and leptin can be observed in a preparation in which synaptic transmission is blocked. Using Fos protein expression to quantify neuronal activation, we have also shown that the hypothalamus is more responsive to GHS/ghrelin in 48-hour fasted rats. This increased responsiveness can be reversed by chronic central infusion of either leptin or insulin. Also refeeding for only two hours at the end of a 48-hour fast reverses the increased responsiveness to GHS, suggesting that central responsiveness to GHS can be regulated acutely, perhaps via some aspect of the feeding process or by absorption of nutrients. We conclude that 1) GHS (and ghrelin) interact with hypothalamic circuits controlling body weight, including leptin- and insulin-sensitive circuits and 2) central responsiveness to GHS is altered by circulating satiety factors and by nutritional state.
机译：最近已被证明克隆GHS受体的生长激素分泌蛋白（GHS）和GHRELIN是克隆GHS受体的内源性配体，以诱导啮齿动物的肥胖。现在，我们一直在调查中央网站和GHS的行动机制，主要是与他们的增长激素释放行动有关。然而，已经清楚地明确表示这些化合物可以激活含有神经肝病Y的神经元，并与控制体重和食欲的下丘脑电路相互作用。 GHS和GHRELIN诱导肥胖，尽管可能无法完全理解这种效果的CNS机制。下丘脑电路调节体重可以容易地识别，因为它们对循环饱腹腹部诸如瘦蛋白和胰岛素的循环饱腹腹膜。因此，在体外电泳 - oglogy研究中，我们已经表明，通过瘦蛋白给药倾向于抑制由GHS激发的细胞。此外，GHS响应细胞似乎是Leptin的直接靶标，因为可以在突触传递被阻断的制备中观察到对GHS和瘦蛋白的这些反应。使用FOS蛋白表达来量化神经元激活，我们还表明，下丘脑对48小时禁食大鼠的GHS / GHRELIN更响应于GHS / GHRELIN。通过瘦蛋白或胰岛素的慢性中央输注可以逆转这种增加的响应性。在48小时的速度结束时也仅改变了两个小时的快速逆转了对GH的响应性增加，这表明可以通过饲养过程的某些方面或通过吸收营养物质来调节对GHS的中心响应性。我们得出结论，通过循环饱腹感因因素和营养状态，GHS（和Ghrelin）与控制体重相互作用，包括控制体重，包括瘦素和胰岛素敏感电路和2）对GHS的中央响应性。

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