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首页> 外文期刊>Neuroscience Letters: An International Multidisciplinary Journal Devoted to the Rapid Publication of Basic Research in the Brain Sciences >AMP-activated protein kinase activates neuropeptide Y neurons in the hypothalamic arcuate nucleus to increase food intake in rats.
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AMP-activated protein kinase activates neuropeptide Y neurons in the hypothalamic arcuate nucleus to increase food intake in rats.

机译：AMP激活的蛋白激酶激活下丘脑弓状核中的神经肽Y神经元，以增加大鼠的食物摄入量。

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摘要

AMP-activated protein kinase (AMPK) is an energy sensor that is activated by the increase of intracellular AMP:ATP ratio. AMPK in the hypothalamic arcuate nucleus (ARC) is activated during fasting and the activation of AMPK stimulates food intake. To clarify the pathway underlying AMPK-induced feeding, we monitored the activity of single ARC neurons by measuring cytosolic Ca(2+) concentration ([Ca(2+)](i)) with fura-2 fluorescence imaging. An AMPK activator, AICA-riboside (AICAR), at 200 muM increased [Ca(2+)](i) in 24% of ARC neurons. AMPK and acetyl CoA carboxylase were phosphorylated in the neurons with [Ca(2+)](i) responses to AICAR. AICAR-induced [Ca(2+)](i) increases were inhibited by Ca(2+)-free condition but not by thapsigargin, suggesting that AICAR increases [Ca(2+)](i) through Ca(2+) influx from extracellular space. Among AICAR-responding ARC neurons, 38% were neuropeptide Y (NPY)-immunoreactive neurons while no proopiomelanocortin (POMC)-immunoreactive neuron was observed. Intracerebroventricular administration of AICAR increased food intake, and the AICAR-induced food intake was abolished by the co-administration of NPY Y1 receptor antagonist, 1229U91. These results indicate that the activation of AMPK leads to the activation of ARC NPY neurons through Ca(2+) influx, thereby causing NPY-dependent food intake. These mechanisms could be implicated in the stimulation of food intake by physiological orexigenic substances.
机译：AMP激活的蛋白激酶（AMPK）是一种能量传感器，可通过增加细胞内AMP：ATP比例来激活。下丘脑弓状核（ARC）中的AMPK在禁食期间被激活，而AMPK的激活则刺激了食物的摄入。为了阐明AMPK诱导进食的基础途径，我们通过测量呋喃2荧光成像测量胞质Ca（2+）浓度（[Ca（2 +）]（i））来监控单个ARC神经元的活性。 AMPK激活剂AICA核糖苷（AICAR）在200μM时可在24％的ARC神经元中增加[Ca（2 +）]（i）。 AMPK和乙酰CoA羧化酶在神经元中被磷酸化，对AICAR的反应为[Ca（2 +）]（i）。 AICAR诱导的[Ca（2 +）]（i）增加受到无Ca（2+）条件的抑制，但不受毒胡萝卜素抑制，这表明AICAR通过Ca（2+）增加[Ca（2 +）]（i）。从细胞外空间流入。在AICAR响应的ARC神经元中，有38％是神经肽Y（NPY）免疫反应性神经元，而没有观察到丙泊黑皮质素（POMC）免疫反应性神经元。脑室内施用AICAR可以增加食物摄入量，并且与NPY Y1受体拮抗剂1229U91并用可以消除AICAR诱导的食物摄入量。这些结果表明AMPK的激活导致通过Ca（2+）涌入的ARC NPY神经元的激活，从而引起NPY依赖性食物的摄入。这些机制可能与生理致病物质刺激食物摄入有关。

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