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Shannon M Bailey, Uduak S Udoh and Martin E Young

Introduction Both energetic supply and demand fluctuate as a function of time-of-day, concomitant with daily sleep–wake and fasting–feeding cycles. It is therefore not surprising that marked diurnal variations in metabolism are observed at multiple

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Che-Pei Kung and Maureen E Murphy

relationship between p53, metabolism and metabolic diseases has become a new focal point for p53 researchers ( Sano et al . 2007 , Vousden & Ryan 2009 , Berkers et al . 2013 ). This review will cover the role of p53 in metabolism, with focus on its role in

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Mariana Rosolen Tavares, Simone Ferreira Lemes, Thais de Fante, Cristina Saenz de Miera, Isadora Carolina Betim Pavan, Rosangela Maria Neves Bezerra, Patricia Oliveira Prada, Marcio Alberto Torsoni, Carol Fuzeti Elias and Fernando Moreira Simabuco

(CNS) for controlling the metabolism of the entire body, being responsible for integrating hormonal and nutritional signals from the periphery and for coordinating appropriate responses associated with the individual nutritional status ( Bouret

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Cátia F Gonçalves and Qing-Jun Meng

their precise spatial and temporal control. Remarkably, physiological functions such as longitudinal bone growth, bone remodelling, chondrocyte metabolism and cartilage matrix turnover exhibit 24-h rhythms, being controlled by the peripheral circadian

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Oliver C Watkins, Mohammed Omedul Islam, Preben Selvam, Reshma Appukuttan Pillai, Amaury Cazenave-Gassiot, Anne K Bendt, Neerja Karnani, Keith M Godfrey, Rohan M Lewis, Markus R Wenk and Shiao-Yng Chan

et al. 2016 ). Perturbations in myo-inositol synthesis, metabolism and excretion have been associated with the insulin-resistant conditions of polycystic ovary syndrome (PCOS), diabetes mellitus and metabolic syndrome ( Croze & Soulage 2013 ), and

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Daniel M Kelly and T Hugh Jones

understood and there are few published papers that have investigated potential mechanisms by which testosterone increases insulin sensitivity and regulates glucose and lipid metabolism. The major insulin-responsive target tissues, such as skeletal muscle

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Sara S Ellingwood and Alan Cheng

. From the glycogen storage diseases (GSDs), congenital disorders arising from mutations in enzymes controlling glycogen metabolism, we have obtained a clear picture in the cellular pathways involved. Along the way, this led to three Nobel prizes in

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Jonathan M Mudry, Julie Massart, Ferenc L M Szekeres and Anna Krook

stores ( Sosic et al . 2003 ). A role for TWIST proteins in metabolism has been proposed in adipose tissue, where TWIST1 is reported to regulate cytokine expression ( Pettersson et al . 2010 ). In adipose cells, TWIST1 silencing reduces fatty acid

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Dawn E W Livingstone, Emma M Di Rollo, Tracy C-S Mak, Karen Sooy, Brian R Walker and Ruth Andrew

 Adrenal gland (mg) 2.3 ± 0.3 2.3 ± 0.3  Thymus (mg) 34.1 ± 2.3 34.9 ± 2.9  Plasma testosterone (pg/mL) 66 ± 10 123 ± 24* Liver glucocorticoid metabolism  11βHSD1 velocity (nmol/mg/h) 20.1 ± 2.3 16

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Fiona Roberts, Greg Markby, Scott Dillon, Colin Farquharson and Vicky E MacRae

, whereby energy metabolism and bone formation regulate one another in a feedback loop. Following recent work which led to the discovery of metabolically active osteocalcin, a hormone secreted specifically by the osteoblast to promote insulin sensitivity