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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Gustavo W Fernandes, Cintia B Ueta, Tatiane L Fonseca, Cecilia H A Gouveia, Carmen L Lancellotti, Patrícia C Brum, Marcelo A Christoffolete, Antonio C Bianco, and Miriam O Ribeiro
B Anguiano, R Rojas-Huidobro, G Delgado, and C Aceves
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
Samira Fargali, Thomas Scherer, Andrew C Shin, Masato Sadahiro, Christoph Buettner, and Stephen R Salton
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
Liisa Ailanen, Suvi T Ruohonen, Laura H Vähätalo, Katja Tuomainen, Kim Eerola, Henriikka Salomäki-Myftari, Matias Röyttä, Asta Laiho, Markku Ahotupa, Helena Gylling, and Eriika Savontaus
(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
Michael Rosenbaum and Rudolph L Leibel
↑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
Iyad H Manaserh, Emily Maly, Marziyeh Jahromi, Lakshmikanth Chikkamenahalli, Joshua Park, and Jennifer Hill
nonshivering thermogenesis ( Oelkrug et al. 2015 ). The sympathetic nervous system (SNS) plays a large role in this process. The SNS activates BAT B3-adrenergic receptors causing higher UCP1 activity and UCP1 gene expression while increasing lipolysis in
Eric D Bruder, Lauren Jacobson, and Hershel Raff
. 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
David E Henley, Fiona Buchanan, Rosemary Gibson, Jennie A Douthwaite, Susan A Wood, Wolfram W Woltersdorf, James R Catterall, and Stafford L Lightman
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
Patricia C Lisboa, Ellen P S Conceição, Elaine de Oliveira, and Egberto G Moura
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
Liping Luo and Meilian Liu
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
