Intermediary Metabolism Group, Center for Neurosciences and Cell Biology of Coimbra , Coimbra , Portugal.
Front Endocrinol (Lausanne). 2013 Aug 15;4:103. doi: 10.3389/fendo.2013.00103. eCollection 2013.
Appetite is regulated by a coordinated interplay between gut, adipose tissue, and brain. A primary site for the regulation of appetite is the hypothalamus where interaction between orexigenic neurons, expressing Neuropeptide Y/Agouti-related protein, and anorexigenic neurons, expressing Pro-opiomelanocortin cocaine/Amphetamine-related transcript, controls energy homeostasis. Within the hypothalamus, several peripheral signals have been shown to modulate the activity of these neurons, including the orexigenic peptide ghrelin and the anorexigenic hormones insulin and leptin. In addition to the accumulated knowledge on neuropeptide signaling, presence and function of amino acid neurotransmitters in key hypothalamic neurons brought a new light into appetite regulation. Therefore, the principal aim of this review will be to describe the current knowledge of the role of amino acid neurotransmitters in the mechanism of neuronal activation during appetite regulation and the associated neuronal-astrocytic metabolic coupling mechanisms. Glutamate and GABA dominate synaptic transmission in the hypothalamus and administration of their receptors agonists into hypothalamic nuclei stimulates feeding. By using (13)C High-Resolution Magic Angle Spinning Nuclear Magnetic Resonance spectroscopy based analysis, the Cerdán group has shown that increased neuronal firing in mice hypothalamus, as triggered by appetite during the feeding-fasting paradigm, may stimulate the use of lactate as neuronal fuel leading to increased astrocytic glucose consumption and glycolysis. Moreover, fasted mice showed increased hypothalamic [2-(13)C]GABA content, which may be explained by the existence of GABAergic neurons in key appetite regulation hypothalamic nuclei. Interestingly, increased [2-(13)C]GABA concentration in the hypothalamus of fasted animals appears to result mainly from reduction in GABA metabolizing pathways, rather than increased GABA synthesis by augmented activity of the glutamate-glutamine-GABA cycle.
食欲受肠道、脂肪组织和大脑的协调作用调节。调节食欲的主要部位是下丘脑,在这里,表达神经肽 Y/Agouti 相关蛋白的食欲神经元与表达 Pro-opiomelanocortin cocaine/Amphetamine 相关转录物的厌食神经元相互作用,控制能量平衡。在下丘脑中,已经证明几种外周信号可以调节这些神经元的活性,包括食欲肽 ghrelin 和厌食激素胰岛素和瘦素。除了对神经肽信号的积累知识外,氨基酸神经递质在关键下丘脑神经元中的存在和功能为食欲调节带来了新的启示。因此,本综述的主要目的将描述氨基酸神经递质在食欲调节期间神经元激活机制中的作用以及相关的神经元-星形胶质细胞代谢偶联机制的最新知识。谷氨酸和 GABA 在下丘脑的突触传递中占主导地位,其受体激动剂在下丘脑核团中的给药会刺激摄食。通过使用基于 (13)C 高分辨率魔角旋转核磁共振波谱的分析,Cerdán 小组表明,如在进食-禁食范式期间由食欲触发的小鼠下丘脑神经元放电增加,可能会刺激使用乳酸作为神经元燃料,导致增加星形胶质细胞葡萄糖消耗和糖酵解。此外,禁食小鼠显示出增加的下丘脑 [2-(13)C]GABA 含量,这可能是由于关键食欲调节下丘脑核团中存在 GABA 能神经元。有趣的是,禁食动物下丘脑 [2-(13)C]GABA 浓度的增加似乎主要是由于 GABA 代谢途径的减少,而不是通过谷氨酸-谷氨酰胺-GABA 循环活性增强导致 GABA 合成增加。