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Luba Sominsky, Ilvana Ziko, Thai-Xinh Nguyen, Julie Quach and Sarah J Spencer

chronically elevated levels of leptin may reduce the sensitivity of leptin receptors, particularly in the ARC, resulting in a resistance to the anorexigenic actions of leptin and further contributing to the maintenance of obesity ( Myers et al . 2008

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Alison Mostyn, Sylvain Sebert, Jennie C Litten, Katharine S Perkins, John Laws, Michael E Symonds and Lynne Clarke

et al. 2005 ). Both actions would reduce circulating leptin and action upon the leptin receptor. The GR is upregulated in vitro by chronic leptin administration, but is conversely downregulated following acute leptin administration ( Gnanalingham

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Qingling Huang, Elena Timofeeva and Denis Richard

mediated at least partially through the VMH, where the leptin receptors are expressed ( Elmquist et al. 1998 a , b , Nishiyama et al. 1999 ). The adipocyte-derived hormone leptin circulates in the blood in proportion to body adiposity ( Zhang

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Katie Wynne, Sarah Stanley, Barbara McGowan and Steve Bloom

, expressing both orexin and leptin receptors, have been identified in the gastrointestinal tract, and appear to be activated during starvation ( Kirchgessner & Liu 1999 ). Orexin is also expressed in the endocrine cells in the gastric mucosa, intestine and

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Giulia Baldini and Kevin D Phelan

, Morton et al. 2014 , Gautron et al. 2015 , Andermann & Lowell 2017 ). In the fed state, leptin also binds to leptin receptors to inhibit secretion of AgRP and of neuropeptide Y (NPY) expressed by AgRP/NPY neurons. Conversely, in the ‘starved state

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B Beck and S Richy

, Kalra et al . 2003 ) and despite the mutation in the leptin receptor gene ( Chua et al . 1996 , Iida et al . 1996 ), the obese Zucker rat is not totally leptin unresponsive. It shows a blunted response after leptin injection ( AlBarazanji et al

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K Rousseau, Z Atcha, J Denton, F R A Cagampang, A R Ennos, A J Freemont and A S I Loudon

leptin receptor expression ( db/db genotype) exhibit a markedly elevated bone mass with increased mineralization and bone formation rate compared with wild-type mice. Intracerebroventricular (i.c.v) infusion of leptin in the ob/ob mice was shown to

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M A L Costa da Veiga, K de Jesus Oliveira, F H Curty and C C Pazos de Moura

the peptide ( Rettori et al. 1992 ). However, it is not known if thyroid hormones are able to modulate leptin or leptin receptor expression at the pituitary. This is a feasible hypothesis since pituitary leptin has been shown to be positively

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Marcela Oliveira, Diego M Assis, Thaysa Paschoalin, Antonio Miranda, Eliane B Ribeiro, Maria A Juliano, Dieter Brömme, Marcelo Augusto Christoffolete, Nilana M T Barros and Adriana K Carmona

chromosome 4. Leptin receptor null mice ( db/db ) exhibit a phenotype similar to that of ob/ob mice, which is used as a model for obesity ( Tartaglia 1997 ). The clearance of leptin by the kidneys is believed to be the end point of leptin action, and the

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Russell T Turner, Kenneth A Philbrick, Amida F Kuah, Adam J Branscum and Urszula T Iwaniec

of bone marrow from leptin receptor-deficient db/db mice, and increased endocortical bone formation in ob/ob mice following leptin administration ( Turner et al . 2013 ). Thus, the reduced cortical thickness in femurs of ob/ob mice could result