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Jessica A Deis, Hong Guo, Yingjie Wu, Chengyu Liu, David A Bernlohr, and Xiaoli Chen

lipolysis to provide fatty acids to support uncoupling of the electron transport chain ( Cao et al . 2001 , 2004 ). However, alternative, non-adrenergic pathways have also been identified as promoting beiging of WAT. The anti-diabetic drug rosiglitazone

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C Folgueira, S Barja-Fernandez, P Gonzalez-Saenz, V Pena-Leon, C Castelao, M Ruiz-Piñon, F F Casanueva, R Nogueiras, and L M Seoane

exert a direct action on human visceral adipocytes stimulating lipolysis through the activation and phosphorylation of HSL and the upregulation of several genes involved in lipid mobilization ( Rodriguez et al . 2016 ). Several studies have shown that

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Andrew Whittle

of its potential substrates ( Misono 2011 ). Lipolysis in adipose tissue following adrenergic stimulation was thought to be solely dependant on cAMP levels, but it has been demonstrated that in white adipocytes, increased cGMP levels following NP

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Ayse Basak Engin, Atilla Engin, and Ipek Isik Gonul

mRNA expression in macrophages through the TLR4/NF-κB pathway. Macrophage-induced adipocyte lipolysis aggravates obesity-induced adipose tissue inflammation by this way ( Ichioka et al. 2011 ). TLR-dependent polarization mediators of M1 macrophages

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Qin He, Dan Mei, Sha Sha, Shanshan Fan, Lin Wang, and Ming Dong

concomitant increase in autophagy flux. It suggested that autophagy may play an absolutely necessary role in lipolysis, which could provide a new way to eliminate lipid accumulation in addition to lipase-mediated lipolysis. Autophagy is regulated by a

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Xu-guang Zhu, Dong Wook Kim, Michael L Goodson, Martin L Privalsky, and Sheue-Yann Cheng

phenotype described here for the TRα1-PV mutation, a TRα1-P398H mutation produced visceral adiposity, hyperleptinemia, reduced sensitivity to catecholamine-stimulated lipolysis, and hepatic steatosis ( Liu et al . 2003 ). These divergent metabolic outcomes

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Guojun Shi, Chen Sun, Weiqiong Gu, Minglan Yang, Xiaofang Zhang, Nan Zhai, Yan Lu, Zhijian Zhang, Peishun Shou, Zhiguo Zhang, and Guang Ning

and regulated gut hormones and motility ( Xiong et al . 2004 , Samuel et al . 2008 ). Then, several other groups argued that FFAR2 rather than FFAR3 inhibited lipolysis and triggered leptin secretion and adipogenesis ( Hong et al . 2005 , Ge et

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Pamela Petrocchi-Passeri, Cheryl Cero, Alessandro Cutarelli, Claudio Frank, Cinzia Severini, Alessandro Bartolomucci, and Roberta Possenti

). The C-terminal internal fragment TLQP-21 – which was originally investigated for its role in energy balance and lipolysis ( Bartolomucci et al . 2006 , 2009 , Fargali et al . 2012 , Possenti et al . 2012 ) – has recently been implicated in

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I J Bujalska, M Quinkler, J W Tomlinson, C T Montague, D M Smith, and P M Stewart

electrolyte homeostasis and lipolysis in human adipocytes was decreased 2.7-fold by cortisol and was below detection levels in SC cells. Common adipose-specific genes Twenty-eight genes were upregulated by cortisol in both

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Stefania Carobbio, Barry Rosen, and Antonio Vidal-Puig

profile and mature brown adipocytes displayed functional properties such as increased lipolysis in response to β-adrenergic stimulation and oxygen consumption levels. Stable, faithful maintenance of both the brown and white adipocyte phenotypes could be