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Fasting mediated increase in p-BAD~(ser155) and p-AKT~(ser473) in the prefrontal cortex of mice

机译:空腹介导的小鼠前额叶皮层中p-BAD〜(ser155)和p-AKT〜(ser473)的增加

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摘要

BAD-deficient mice and fasting have several common functional roles in seizures, beta-hydroxybutyrate (BHB) uptake in brain and alteration in counterregulatory hormonal regulation during hypoglycemia. Neuronal specific insulin receptor knockout (NIRKO) mice display impaired counterregulatory hormonal responses during hypoglycemia. In this study we investigated the fasting mediated expression of p-BAD~(ser155) and p-AKT~(ser473) in different regions of brain (prefrontal cortex, hippocampus, midbrain and hypothalamus). Fasting specifically increases p-BAD~(ser155) and p-AKT~(ser473) in prefrontal cortex and decreases in other regions of brain. Our results suggest that fasting may increase the uptake BHB by decreasing p-BAD~(ser155) in the brain during hypoglycemia except prefrontal cortex and it uncovers specific functional area of p-BAD~(ser155) and p-AKT~(se'473) that may regulates counter regulatory hormonal response. Overall in support with previous findings, fasting mediated hypoglycemia activates prefrontal cortex insulin signaling which influences the hypothalamic paraventricular nucleus mediated activation of sympathoadrenal hormonal responses.
机译:BAD缺陷小鼠和禁食在癫痫发作,大脑中β-羟丁酸(BHB)摄取以及低血糖期间反调节激素调节的改变中具有几种常见的功能。低血糖期间,神经元特异性胰岛素受体敲除(NIRKO)小鼠显示出受损的反调节激素反应。在这项研究中,我们调查了禁食介导的p-BAD〜(ser155)和p-AKT〜(ser473)在大脑不同区域(前额叶皮层,海马,中脑和下丘脑)的表达。禁食会特别增加前额叶皮层中的p-BAD〜(ser155)和p-AKT〜(ser473),并在其他大脑区域减少。我们的研究结果表明,空腹可能通过降低除前额叶皮层以外的低血糖患者大脑中的p-BAD〜(ser155)来增加BHB的摄取,并且它揭示了p-BAD〜(ser155)和p-AKT〜(se'473)的特定功能区域),可能会调节荷尔蒙的反调节。总的来说,支持先前的发现,空腹介导的低血糖会激活前额叶皮质胰岛素信号传导,从而影响下丘脑室旁核介导的交感肾上腺激素反应的激活。

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