Nutritional, endocrine, and neurological signals converge in multiple brain centres to control feeding behaviour and food intake as part of the allostatic regulation of energy balance. Among the several neuroendocrine systems involved, the leptin, glucocorticoid, and glucagon-like peptide 1 (GLP1) systems have been extensively researched. Leptin is at the top hierarchical level since its complete absence is sufficient to trigger severe hyperphagia. Glucocorticoids are key regulators of the energy balance adaptation to stress and their sustained excess leads to excessive adiposity and metabolic perturbations. GLP1 participates in metabolic adaptation to food intake, regulating insulin secretion and satiety by parallel central and peripheral signalling systems. Herein, we review the brain and peripheral targets of these three hormone systems that integrate to regulate food intake, feeding behaviour, and metabolic homeostasis. We examine the functional relationships between leptin, glucocorticoids, and GLP1 at the central and peripheral levels, including the cross-regulation of their circulating levels and their cooperative or antagonistic actions at different brain centres. The pathophysiological roles of these neuroendocrine systems in dysregulated intake are explored in the two extremes of body adiposity – obesity and lipodystrophy – and eating behaviour disorders.

中文翻译：

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瘦素、糖皮质激素和 GLP1 之间的相互作用调节食物摄入和进食行为

营养、内分泌和神经信号汇聚在多个大脑中心，以控制进食行为和食物摄入，作为能量平衡的非稳态调节的一部分。在涉及的几个神经内分泌系统中，瘦素、糖皮质激素和胰高血糖素样肽1 (GLP1) 系统已被广泛研究。瘦素处于最高层次，因为它的完全缺失足以引发严重的食欲过盛。糖皮质激素是适应压力的能量平衡的关键调节剂，其持续过量会导致过度肥胖和代谢紊乱。GLP1 参与食物摄入的代谢适应，通过平行的中枢和外周信号系统调节胰岛素分泌和饱腹感。在此，我们回顾了这三种激素系统的大脑和外周靶标，这些激素系统整合起来调节食物摄入、进食行为和代谢稳态。我们研究了瘦素、糖皮质激素和 GLP1 在中枢和外周水平上的功能关系，包括它们循环水平的交叉调节以及它们在不同大脑中心的合作或拮抗作用。这些神经内分泌系统在摄入失调中的病理生理学作用在身体肥胖的两个极端——肥胖和脂肪营养不良——以及饮食行为障碍中进行了探索。