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( Sotiropoulos et al . 2006 ). Acute administration of GH regulates muscle mitochondrial function by increasing the levels of several key mitochondrial proteins, and by switching fuel utilization toward fat oxidation ( Short et al . 2008 ). In addition
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area. The animals were maintained under constant conditions for 2 or more weeks to allow for their endogenous circadian rhythms to ‘free-run’. During this time, the animals continued to have consolidated sleep/wake cycles. These were monitored using
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( Lincoln & Short 1980 ). Similarly, there is a nocturnal rise in Prl in man ( Arendt 1988 , Thorner et al. 1992 ) although some studies have attributed this to the occurrence of sleep rather than the concomitant elevation in melatonin levels ( Sassin et
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circadian glucocorticoid rhythm is altered in several pathological states; e.g. major depressive disorder ( Sachar et al. 1973 , Linkowski et al. 1985 , Pfohl et al. 1985 ), Alzheimer’s disease, sleep deprivation ( Spiegel et al. 1999 ), and normal
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prolonged hexobarbital-induced sleep time that was still ~30% shorter than that resulting from the MSG-alone treatment and CYP2C11 expression levels (mRNA and protein) representing ~40% of controls. Evidently, even though there was no circulating GH after 12
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therefore characterised the metabolic phenotype of the PWS-IC del model in this study, quantifying appetitive and consummatory feeding behaviour, lipid profiling and storage, short-term responses to high-fat diet exposure and assessment of thermogenic
Pinnacle Clinical Research, Live Oak, USA
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overconsumption, in addition to causing weight gain and/or obesity if chronically overconsumed, can lead to disruptions in sleep-wake cycles, increased risk for non-alcoholic fatty liver disease (NAFLD) and insulin resistance ( Flowers & Ntambi 2009 , He et al
Centre for Paediatrics and Child Health, Department of Paediatric Endocrinology, Department of Endocrinology, Centre for Endocrinology and Diabetes, Institute of Human Development, Faculty of Medical and Human Sciences, University of Manchester, M13 9WL, UK
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Centre for Paediatrics and Child Health, Department of Paediatric Endocrinology, Department of Endocrinology, Centre for Endocrinology and Diabetes, Institute of Human Development, Faculty of Medical and Human Sciences, University of Manchester, M13 9WL, UK
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Centre for Paediatrics and Child Health, Department of Paediatric Endocrinology, Department of Endocrinology, Centre for Endocrinology and Diabetes, Institute of Human Development, Faculty of Medical and Human Sciences, University of Manchester, M13 9WL, UK
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inhibitory factor. The evolution in understanding the central GH axis The ‘early’ years: 1920s–1960s The lack of a growth-stimulating factor in humans who exhibited severe proportionate short stature has been recognised throughout history. However, the
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temperature, hormones release and sleep–wake cycles ( Coomans et al. 2015 , Kingsbury et al. 2016 ). Meanwhile, peripheral cells in the heart, liver and pancreas also contain intrinsic circadian oscillators ( Pezuk et al. 2010 , Podobed et al. 2014
Department of Endocrinology, CI Parhon National Institute of Endocrinology, Department of Endocrinology, Carol Davila University of Medicine and Pharmacy, Bucharest, Romania
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symptoms onset to diagnosis is usually about 7–10 years ( Rajasoorya et al . 1994 ), at the time of diagnosis many patients present with specific complications of the disease. The most prevalent comorbidities are arterial hypertension, sleep apnea