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Systemic glucocorticoid excess causes several adverse metabolic conditions, most notably Cushing’s syndrome. These effects are amplified by the intracellular enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1). Here we determined the less well characterised effects of glucocorticoid excess, and the contribution of 11β-HSD1 amplification, on metabolic rate in mice. Male and female C57BL/6J (wild type, WT) and 11β-HSD1 knock out (11β-HSD1KO) mice were treated with high-dose corticosterone or a vehicle control for 3 weeks. Indirect calorimetry was conducted during the final week of treatment, with or without fasting, to determine the impact on metabolic rate. We found that corticosterone treatment elevated metabolic rate and promoted carbohydrate utilisation primarily in female WT mice, with effects more pronounced during the light phase. Corticosterone treatment also resulted in greater fat accumulation in female WT mice. Corticosterone induced hyperphagia was identified as a likely causal factor altering the respiratory exchange ratio (RER) but not energy expenditure (EE). Male and female 11β-HSD1KO mice were protected against these effects. We identify novel metabolic consequences of sustained glucocorticoid excess, identify a key mechanism of hyperphagia and demonstrate that 11β-HSD1 is required to manifest the full metabolic derangement.
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resting metabolic rate. They can tolerate the resulting severe decrease in body temperature and thereby save large amounts of energy (up to 98%). Different forms of metabolic depression exist, ranging from obligate, deep hibernation, characterized by 96
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decrease in basal metabolic rate ( Ravucin et al . 1985 , Rosenbaum et al . 2002 ). The responses to food restriction have been well documented in a number of species, including humans ( Kelley et al . 1993 ), monkeys ( Kemnitz et al . 1994 ), rats
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-induced thermogenesis in Pacap −/− mice Pacap −/− and Pacap +/+ mice were paired and housed together according to age and gender. Resting and maximal metabolic rates (MMR) were measured in 8-week-old mice reared at 24 °C. These mice were then acclimated at 18 °C
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Department of Cellular and Integrative Physiology, Section of Nephrology, Department of Internal Medicine, University of Nebraska Medical Center, 985850 Nebraska Medical Center, Omaha, Nebraska 68198-5850, USA
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with WT mice on high-fat diet ( n =7–8). Basal metabolic rate and energy expenditure are decreased in Parp -KO mice. (B) Comparison of the oxygen consumption for a period of 24 h for WT and Parp -KO mice that were fed HF diet for 19 weeks. (C
Department of Translational Medicine, EPM, Federal University of Sao Paulo, Sao Paulo, SP, Brazil
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Department of Translational Medicine, EPM, Federal University of Sao Paulo, Sao Paulo, SP, Brazil
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Introduction A balance between food intake and energy expenditure is essential to preserve fuel homeostasis. Changes in caloric intake trigger physiological responses that include adaptive modifications in appetite, metabolic rate and energy
Biological Science Course, Division of Endocrinology, Department of Anatomy, Department of Cell and Developmental Biology, Lipids Laboratory (LIM 10) Faculty of Medical Sciences, Clinical Emergency, School of Arts, AFIP and Pathology, CCBS, Presbyterian University Mackenzie, Rua da Consolação, 930 Prédio 38, Curso de Biologia, São Paulo, SP 01302-907, Brazil
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Biological Science Course, Division of Endocrinology, Department of Anatomy, Department of Cell and Developmental Biology, Lipids Laboratory (LIM 10) Faculty of Medical Sciences, Clinical Emergency, School of Arts, AFIP and Pathology, CCBS, Presbyterian University Mackenzie, Rua da Consolação, 930 Prédio 38, Curso de Biologia, São Paulo, SP 01302-907, Brazil
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period, animals were studied for resting metabolic rate (RMR), glucose tolerance test (GTT), and insulin tolerance test (ITT). Animals were subsequently killed by exsanguinations under urethane anesthesia, and blood processed for plasma isolation and
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Laboratório de Fisiologia Endócrina Doris Rosenthal, Laboratório de Biologia do Exercício, Instituto de Biofísica Carlos Chagas Filho and Instituto de Pesquisa Translacional em Saúde e Ambiente na Região Amazônica (INPeTAM), CCS-Bloco G- Cidade Universitria, Ilha do Fundo, Rio de Janeiro 21949-900, Brazil
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Introduction Compound 3,3′,5-triiodothyronine (T 3 ) exerts many important effects on the basal metabolic rate and increases oxygen consumption. Several years ago, it was shown that 3,5-diiodothyronine (3,5-T2) is responsible for certain non
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Institute of Medical Science, Department of Psychology, University of Toronto, Toronto, Ontario, Canada M5S 3G3
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have marked increases in diaphorase staining of muscle fibers, suggestive of hypermetabolism ( Monks et al . 2007 ). Indeed, HSA-AR rats exhibit increased resting metabolic rate (RMR) as well as increased electron transport chain (ETC) activity within
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increased metabolic rate, increased locomotor activity or both ( Shimada et al. 1998 , Segal-Lieberman et al. 2003 ). MCH is expressed in the central nervous system (CNS), primarily in the rostral zona incerta/incerto-hypothalamic and the lateral