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Christopher E Wall, Ruth T Yu, Anne R Atkins, Michael Downes, and Ronald M Evans

fatty acids that can originate from dietary sources, lipolysis of lipid storage in adipose tissues, or de novo lipogenesis ( Dreyer et al . 1993 ). While PPARδ is responsible for regulating its target genes most critically in skeletal muscle, PPARα

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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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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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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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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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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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Jan Wilde, Maria Erdmann, Michael Mertens, Gabriele Eiselt, and Martin Schmidt

content in adipose tissue surrounding breast tumors ( Meng et al . 2001 ). These cytokines, e.g. TNFα, via the induction of insulin resistance, also stimulate lipolysis in adipocytes ( Uysal et al . 1997 ). As local lipolysis is the most likely source of

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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