Neuroendocrine Circuits Governing Energy Balance and Stress Regulation: Functional Overlap and Therapeutic Implications  Yvonne M. Ulrich-Lai, Karen K.

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Neuroendocrine Circuits Governing Energy Balance and Stress Regulation: Functional Overlap and Therapeutic Implications  Yvonne M. Ulrich-Lai, Karen K. Ryan  Cell Metabolism  Volume 19, Issue 6, Pages 910-925 (June 2014) DOI: 10.1016/j.cmet.2014.01.020 Copyright © 2014 Elsevier Inc. Terms and Conditions

Figure 1 Canonical Pathways that Regulate Stress Responses and Energy Balance For the stress system, information from brainstem and limbic forebrain areas converges in the PVN, which directly activates the HPA axis and regulates autonomic nervous system responses via projections to brainstem. For energy balance, information from brainstem and limbic forebrain areas converge on the ARC, which regulates energy intake and expenditure via connections to the PVN, LHA, and brainstem. Cell Metabolism 2014 19, 910-925DOI: (10.1016/j.cmet.2014.01.020) Copyright © 2014 Elsevier Inc. Terms and Conditions

Figure 2 Schematic Illustrating the Complex Functional Interactions between Homeostatic Metabolic Signaling, Physiological Responses to Stress, and Reward-Driven Food Intake These interactions likely occur, at least in part, as consequence of these systems’ largely overlapping anatomical circuitry. Metabolic signals, including leptin and ghrelin, influence reward-driven food intake—which in turn alters energy balance. These metabolic signals also modulate HPA and autonomic responses to stress. Moreover, stress mediators can override metabolic homeostasis to redistribute fuels in the face of a challenge. Finally, stress mediators like glucocorticoids promote reward-driven food intake, which reciprocally reduces stress responses. All of these systems are profoundly influenced by stress exposure. In stress-prone individuals, this results in increased motivation for food reward and increased intake of highly palatable foods that in turn limit uncomfortable psychological and physiological responses to stress. However, over the long term, chronic stress exposure can contribute to the development of metabolic disease. Cell Metabolism 2014 19, 910-925DOI: (10.1016/j.cmet.2014.01.020) Copyright © 2014 Elsevier Inc. Terms and Conditions