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The adipocyte-derived hormone leptin acts in the brain as part of a negative feedback mechanism to control adiposity by inhibiting food intake and increasing energy expenditure through stimulation of sympathetic nerve activity (SNA). Leptin increases SNA to several distinct beds that are directly or indirectly involved in the regulation of energy homeostasis. This includes white adipose tissue, the liver, kidneys and vasculature. The arcuate nucleus (ARC) contains multiple unique leptin receptor (LepR) positive neuronal populations including those expressing proopiomelanocortin (POMC) and agouti-related peptide (AgRP). In the present study, Bell et al. investigated the role of POMC and AgRP neurons in underlying the autonomic effects of leptin. For this, they analyzed the ability of leptin to increase SNA and parasympathetic nerve activity PSNA subserving various beds in mice lacking the LepR in either POMC or AgRP neurons. Their data show that POMC and AgRP neurons differentially contribute to leptin control of regional activity of the autonomic nervous system. These findings support the notion that leptin engages different neuronal populations in a selective manner to control the activity of the sympathetic and parasympathetic nervous systems.

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In this section authors briefly report on their work recently published in Molecular Metabolism.

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Landon Wood, Darleen Sandoval
University of Michigan, Ann Arbor, USA
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