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energy expenditure and address the current high prevalence of obesity. In mice, BAT develops during the 3-day window E16.5–18.5 ( Hall et al . 2010 ) and after birth can be activated by the sympathetic nervous system (SNS) through stimulation of β
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Departments of, Neuroscience, Medicine, Geriatrics, Box 1065, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, New York 10029, USA
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Departments of, Neuroscience, Medicine, Geriatrics, Box 1065, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, New York 10029, USA
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Introduction The sympathetic nervous system (SNS) is an important regulator of glucose and fat metabolism, and its dysfunction can predispose to obesity and type 2 diabetes mellitus. The melanocortin pathway projects from the hypothalamic
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sympathetic nervous system (SNS) and prolactin (PRL) have been frequently implicated as synergistic and antagonistic influences upon the effects of TH and viceversa. TH antagonizes PRL action by inhibiting the synthesis of the signal transducer and activator
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(WAT) (Egawa et al. 1991, Zarjevski et al. 1993, Shi et al. 2013). An important source of NPY in the periphery is the sympathetic nervous system (SNS), and NPY levels are increased upon stress (Ekblad et al. 1984). Consistently, NPY has been
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↑GH Autonomics ↑↑PNS and ↓↓SNS ↑PNS and ↓SNS a Energy intake ↓↓Satiation Less↓↓Satiation a ↑Hunger a Less↑Hunger a REE, resting energy expenditure; NREE, non-resting energy expenditure; RER, respiratory exchange ratio; T 3 , triiodothyronine; T 4
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Department of Biochemistry and Molecular Biology, University of New Mexico Health Sciences Center, Albuquerque, New Mexico, USA
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during fasting is also responsible for the activation of cAMP-dependent protein kinase A (PKA) pathway and lipolysis in adipocytes. Meanwhile, catecholamine released by sympathetic nervous system (SNS) is also stimulated by fasting, binds to β
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dissipate energy and generate heat in rodents. The ablation of UCP1 gene is able to induce obesity without hyperphagia ( Lowell et al . 1993 ). The UCP1 mRNA expression is stimulated by the sympathetic nervous system (SNS) and leptin via the SNS ( Commins
Henry Wellcome Laboratories for Integrative Neuroscience and Endocrinology, Faculty of Medicine, Clinical Biochemistry, University of Bristol, Bristol BS1 3NY, UK
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system (SNS) hyperactivity is well documented in OSA with high sympathetic drive present across the 24-h period, even during daytime wakefulness and there is a reduction following CPAP ( Narkiewicz & Somers 2003 ). Chronic SNS activation may indirectly
Center for Neuropharmacology and Neurosciences, Albany Medical College, Albany, New York 12208, USA
Department of Medicine, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, USA
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Center for Neuropharmacology and Neurosciences, Albany Medical College, Albany, New York 12208, USA
Department of Medicine, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, USA
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Center for Neuropharmacology and Neurosciences, Albany Medical College, Albany, New York 12208, USA
Department of Medicine, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, USA
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. 2004 ). Catecholamine release from the sympathetic nervous system (SNS) may be a mediator of these responses ( Young 2000 ). A previous study found that the transcription of the human leptin gene is activated by hypoxia, via the transcription factor
Department of Pharmacology, Turku Centre for Biotechnology, Drug Research Doctoral Program, Heart Center, Unit of Clinical Pharmacology, Drug Development and Therapeutics and Turku Center for Disease Modeling, University of Turku, Kiinamyllynkatu 10, 20520 Turku, Finland
Department of Pharmacology, Turku Centre for Biotechnology, Drug Research Doctoral Program, Heart Center, Unit of Clinical Pharmacology, Drug Development and Therapeutics and Turku Center for Disease Modeling, University of Turku, Kiinamyllynkatu 10, 20520 Turku, Finland
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Department of Pharmacology, Turku Centre for Biotechnology, Drug Research Doctoral Program, Heart Center, Unit of Clinical Pharmacology, Drug Development and Therapeutics and Turku Center for Disease Modeling, University of Turku, Kiinamyllynkatu 10, 20520 Turku, Finland
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Department of Pharmacology, Turku Centre for Biotechnology, Drug Research Doctoral Program, Heart Center, Unit of Clinical Pharmacology, Drug Development and Therapeutics and Turku Center for Disease Modeling, University of Turku, Kiinamyllynkatu 10, 20520 Turku, Finland
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Department of Pharmacology, Turku Centre for Biotechnology, Drug Research Doctoral Program, Heart Center, Unit of Clinical Pharmacology, Drug Development and Therapeutics and Turku Center for Disease Modeling, University of Turku, Kiinamyllynkatu 10, 20520 Turku, Finland
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cerebroventricular system produces hypertensive effects, most studies report that α-MSH administration into the NTS decreases blood pressure and heart rate (HR) through a reduced sympathetic nervous system (SNS) activity ( Li et al . 1996 , Pavia et al . 2003