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Bo Zhou, Huixia Li, Jiali Liu, Lin Xu, Qinyue Guo, Hongzhi Sun, and Shufang Wu

476 – 491 . ( doi:10.1016/j.cell.2007.08.047 ). Stralfors P Honnor RC 1989 Insulin-induced dephosphorylation of hormone-sensitive lipase: correlation with lipolysis and cAMP-dependent protein kinase activity . European Journal of Biochemistry

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Carolina Gustavsson, Tomoyoshi Soga, Erik Wahlström, Mattias Vesterlund, Alireza Azimi, Gunnar Norstedt, and Petra Tollet-Egnell

. 2005 ) and antioxidant ( Louet et al . 2004 , Baba et al . 2005 , Borrás et al . 2005 ) properties. Oestrogens have also been shown to inhibit lipogenesis and stimulate lipolysis in abdominal visceral fat depots, to promote use of lipid as a fuel

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Davids Fridmanis, Ramona Petrovska, Dace Pjanova, Helgi B Schiöth, and Janis Klovins

, Kovalitskaia et al . 2008 ). In the adrenal cortex, MC2R affects glucocorticoid production ( Clark & Cammas 1996 ) and synthesis of its own mRNA ( Naville et al . 1999 ). Research with mouse adipocytes has shown that MC2R participates in lipolysis ( Boston

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Kazuyoshi Ukena, Tomohiro Osugi, Jérôme Leprince, Hubert Vaudry, and Kazuyoshi Tsutsui

-induced lipolysis ( Malumba et al . 2010 ). As 3T3-L1 cells express the QRFPR-encoding gene, it appears that 26RFa/QRFP may act in an autocrine/paracrine manner to regulate adipogenesis ( Malumba et al . 2010 ). According to Alonzeau et al . (2013) , 26RFa

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Edwin J W Geven, Folkert Verkaar, Gert Flik, and Peter H M Klaren

, Schreck 2000 ). Cortisol stimulates gluconeogenesis and lipolysis ( Sheridan 1988 , van der Boon et al. 1991 ), which result in increased plasma glucose and free fatty acid levels. These catabolic actions of cortisol reflect its glucocorticoid potency

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J H Duncan Bassett and Graham R Williams

hormone receptors . Bone 36 607 – 616 . Liu YY Schultz JJ Brent GA 2003 A thyroid hormone receptor alpha gene mutation (P398H) is associated with visceral adiposity and impaired catecholamine-stimulated lipolysis in mice . Journal of

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Sofia A Rahman, Azizun Nessa, and Khalid Hussain

inappropriate release leads to persistent hyperinsulinaemic hypoglycaemia (HH). This drives glucose into the insulin sensitive tissues and simultaneously suppresses lipolysis and ketogenesis. The combined hypoketonaemic and hypoglycaemic characteristic of CHI

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Changxue Lu and Sheue-Yann Cheng

H-mutated TRα1 manifest visceral obesity, hyperleptinemia, reduced catecholamine-stimulated lipolysis in WAT, and hepatic steatosis ( Liu et al . 2007 ). In the absence of T 3 , wild-type TRα1 and P398H mutant significantly reduce PPARα

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Jin-Seung Choung, Young-Sun Lee, and Hee-Sook Jun

lipolysis and free fatty acid utilization, contributing to the activation of UCP-1. β 3 -adrenergic receptors are thought to play a role in thermogenesis in brown fat and skeletal muscle, induce adaptive non-shivering thermogenesis and stimulate UCP1

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L J Moran, P A Mundra, H J Teede, and P J Meikle

metabolic effects including suppression of lipogenesis and enhancement of lipolysis ( Shirouchi et al . 2007 ). Elevated lysophosphatidylcholine may indicate an increase in phospholipase activity which is highly expressed in the atherogenic plaque and