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首页> 外文期刊>Cell metabolism >Hypoglycemia-Activated GLUT2 Neurons of the Nucleus Tractus Sotitarius Stimulate Vagal Activity and Gfucagon Secretion
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Hypoglycemia-Activated GLUT2 Neurons of the Nucleus Tractus Sotitarius Stimulate Vagal Activity and Gfucagon Secretion

机译：低血糖激活的Stitarius核的GLUT2神经元刺激迷走神经活性和胰高血糖素的分泌。

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Glucose-sensing neurons in the brainstem participate in the regulation of energy homeostasis but have been poorly characterized because of the lack of specific markers to identify them. Here we show that GLUT2-expressing neurons of the nucleus of the tractus solitarius form a distinct population of hypoglycemia-activated neurons. Their response to low glucose is mediated by reduced intracellular glucose metabolism, increased AMP-activated protein kinase activity, and closure of leak K~+ channels. These are GABAergic neurons that send projections to the vagal motor nucleus. Light-induced stimulation of channelrhodospin-expressing GLUT2 neurons in vivo led to increased parasympathetic nerve firing and glucagon secretion. Thus GLUT2 neurons of the nucleus tractus solitarius link hypoglycemia detection to counterregulatory response. These results may help identify the cause of hypoglycemia-associated autonomic failure, a major threat in the insulin treatment of diabetes.
机译：脑干中的葡萄糖感应神经元参与能量稳态的调节，但由于缺乏识别它们的特异性标记，因此其表征较差。在这里，我们显示孤岛核表达GLUT2的神经元形成了低血糖激活神经元的独特群体。它们对低葡萄糖的反应是通过减少细胞内葡萄糖代谢，增加AMP激活的蛋白激酶活性和关闭K +通道来介导的。这些是GABA能神经元，向迷走神经运动核发送投射信号。光诱导的体内表达通道hodospin的GLUT2神经元的刺激导致副交感神经放电和胰高血糖素分泌增加。因此，孤束核的GLUT2神经元将低血糖检测与反调节反应联系起来。这些结果可能有助于确定低血糖相关的自主神经功能衰竭的原因，这是糖尿病胰岛素治疗的主要威胁。

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