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Nava Chapnik Robert H. Smith Faculty of Agriculture, Fritz Haber Center for Molecular Dynamics, Food and Environment, Institute of Biochemistry, Food Science and Nutrition, The Hebrew University of Jerusalem, Rehovot 76100, Israel

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Yoni Genzer Robert H. Smith Faculty of Agriculture, Fritz Haber Center for Molecular Dynamics, Food and Environment, Institute of Biochemistry, Food Science and Nutrition, The Hebrew University of Jerusalem, Rehovot 76100, Israel

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Avraham Ben-Shimon Robert H. Smith Faculty of Agriculture, Fritz Haber Center for Molecular Dynamics, Food and Environment, Institute of Biochemistry, Food Science and Nutrition, The Hebrew University of Jerusalem, Rehovot 76100, Israel
Robert H. Smith Faculty of Agriculture, Fritz Haber Center for Molecular Dynamics, Food and Environment, Institute of Biochemistry, Food Science and Nutrition, The Hebrew University of Jerusalem, Rehovot 76100, Israel

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Masha Y Niv Robert H. Smith Faculty of Agriculture, Fritz Haber Center for Molecular Dynamics, Food and Environment, Institute of Biochemistry, Food Science and Nutrition, The Hebrew University of Jerusalem, Rehovot 76100, Israel
Robert H. Smith Faculty of Agriculture, Fritz Haber Center for Molecular Dynamics, Food and Environment, Institute of Biochemistry, Food Science and Nutrition, The Hebrew University of Jerusalem, Rehovot 76100, Israel

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Oren Froy Robert H. Smith Faculty of Agriculture, Fritz Haber Center for Molecular Dynamics, Food and Environment, Institute of Biochemistry, Food Science and Nutrition, The Hebrew University of Jerusalem, Rehovot 76100, Israel

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those with normal kidney function. Recent findings indicate that metformin and thiazolidinediones indirectly activate the AMP-activated protein kinase (AMPK; Batandier et al . 2006 ). Direct activation of AMPK has been highlighted as a potential novel

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-13-0625
Volume/Issue:
Volume 221: Issue 1
Free access
Nami Kim Department of Anatomy, Department of Medicine, Integrated Metabolomics Research Group, Department of Life Science, Korea University College of Medicine, Seoul 136-701, South Korea
Department of Anatomy, Department of Medicine, Integrated Metabolomics Research Group, Department of Life Science, Korea University College of Medicine, Seoul 136-701, South Korea

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Jung Ok Lee Department of Anatomy, Department of Medicine, Integrated Metabolomics Research Group, Department of Life Science, Korea University College of Medicine, Seoul 136-701, South Korea

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Hye Jeong Lee Department of Anatomy, Department of Medicine, Integrated Metabolomics Research Group, Department of Life Science, Korea University College of Medicine, Seoul 136-701, South Korea

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Yong Woo Lee Department of Anatomy, Department of Medicine, Integrated Metabolomics Research Group, Department of Life Science, Korea University College of Medicine, Seoul 136-701, South Korea

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Hyung Ip Kim Department of Anatomy, Department of Medicine, Integrated Metabolomics Research Group, Department of Life Science, Korea University College of Medicine, Seoul 136-701, South Korea

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Su Jin Kim Department of Anatomy, Department of Medicine, Integrated Metabolomics Research Group, Department of Life Science, Korea University College of Medicine, Seoul 136-701, South Korea

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Sun Hwa Park Department of Anatomy, Department of Medicine, Integrated Metabolomics Research Group, Department of Life Science, Korea University College of Medicine, Seoul 136-701, South Korea

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Chul Su Lee Department of Anatomy, Department of Medicine, Integrated Metabolomics Research Group, Department of Life Science, Korea University College of Medicine, Seoul 136-701, South Korea

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Sun Woo Ryoo Department of Anatomy, Department of Medicine, Integrated Metabolomics Research Group, Department of Life Science, Korea University College of Medicine, Seoul 136-701, South Korea

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Geum-Sook Hwang Department of Anatomy, Department of Medicine, Integrated Metabolomics Research Group, Department of Life Science, Korea University College of Medicine, Seoul 136-701, South Korea
Department of Anatomy, Department of Medicine, Integrated Metabolomics Research Group, Department of Life Science, Korea University College of Medicine, Seoul 136-701, South Korea

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Hyeon Soo Kim Department of Anatomy, Department of Medicine, Integrated Metabolomics Research Group, Department of Life Science, Korea University College of Medicine, Seoul 136-701, South Korea

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-independent manner. AMP-activated protein kinase (AMPK) is activated during exercise and promotes glucose uptake in the absence of insulin ( Hayashi et al . 1997 ). Impairment of glucose uptake in the muscles is observed in pathological conditions such as obesity

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-15-0302
Volume/Issue:
Volume 228: Issue 2
Open access
Manon M Roustit
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Joan M Vaughan Department of Comparative Biomedical Sciences, Laboratory of Neuronal Structure and Function, Queen's Medical Research Institute, Royal Veterinary College, University of London, Royal College Street, London NW1 0TU, UK

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Pauline M Jamieson Department of Comparative Biomedical Sciences, Laboratory of Neuronal Structure and Function, Queen's Medical Research Institute, Royal Veterinary College, University of London, Royal College Street, London NW1 0TU, UK

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Mark E Cleasby
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muscle ( Chen et al . 2006 ). Furthermore, CRF stimulates muscle substrate oxidation through the activation of both phosphoinositol 3-kinase (PI3K) and AMP-activated protein kinase (AMPK) pathways ( Solinas et al . 2006 ). Investigations into the role

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-14-0181
Volume/Issue:
Volume 223: Issue 2
Open access
Noelia Martínez-Sánchez Department of Physiology, CIMUS, University of Santiago de Compostela-Instituto de Investigación Sanitaria, Santiago de Compostela, Spain
CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), Santiago de Compostela, Spain

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José M Moreno-Navarrete CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), Santiago de Compostela, Spain
Department of Diabetes, Endocrinology and Nutrition, Hospital de Girona ‘Dr Josep Trueta’, Institut D’investigació Biomèdica de Girona (IdIBGi) and University of Girona, Girona, Spain

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Cristina Contreras Department of Physiology, CIMUS, University of Santiago de Compostela-Instituto de Investigación Sanitaria, Santiago de Compostela, Spain
CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), Santiago de Compostela, Spain

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Eva Rial-Pensado Department of Physiology, CIMUS, University of Santiago de Compostela-Instituto de Investigación Sanitaria, Santiago de Compostela, Spain
CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), Santiago de Compostela, Spain

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Johan Fernø Department of Physiology, CIMUS, University of Santiago de Compostela-Instituto de Investigación Sanitaria, Santiago de Compostela, Spain
Department of Clinical Science, KG Jebsen Center for Diabetes Research, University of Bergen, Bergen, Norway

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Rubén Nogueiras Department of Physiology, CIMUS, University of Santiago de Compostela-Instituto de Investigación Sanitaria, Santiago de Compostela, Spain
CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), Santiago de Compostela, Spain

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Carlos Diéguez Department of Physiology, CIMUS, University of Santiago de Compostela-Instituto de Investigación Sanitaria, Santiago de Compostela, Spain
CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), Santiago de Compostela, Spain

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José-Manuel Fernández-Real CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), Santiago de Compostela, Spain
Department of Diabetes, Endocrinology and Nutrition, Hospital de Girona ‘Dr Josep Trueta’, Institut D’investigació Biomèdica de Girona (IdIBGi) and University of Girona, Girona, Spain

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Miguel López Department of Physiology, CIMUS, University of Santiago de Compostela-Instituto de Investigación Sanitaria, Santiago de Compostela, Spain
CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), Santiago de Compostela, Spain

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). Recent evidence from our group has also shown a homeostatic link between the central effects of THs on hypothalamic AMP-activated protein kinase (AMPK), sympathetic tone and UCP1 expression in BAT ( Lopez et al . 2010 , Alvarez-Crespo et al . 2016

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-16-0425
Volume/Issue:
Volume 232: Issue 2
Open access
Ulrika Bergström Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden
Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden

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Charlotte Lindfors Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden
Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden

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Marie Svedberg Department of Clinical Neuroscience, Center for Psychiatric Research, Karolinska Institutet, Stockholm, Sweden

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Jeanette E Johansen Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden
Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden

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Jenny Häggkvist Department of Clinical Neuroscience, Center for Psychiatric Research, Karolinska Institutet, Stockholm, Sweden

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Martin Schalling Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden
Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden

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Rolf Wibom Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden

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Abram Katz Department of Physical Therapy, Ariel University, Ariel, Israel

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Ida A K Nilsson Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden
Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden

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) expressing populations that are anorexigenic ( Grill & Kaplan 2002 , Hillebrand et al . 2002 , Morton et al . 2006 , Schwartz 2006 ). Additionally, hypothalamic AMP-dependent protein kinase (AMPK), a sensor of cellular metabolism that responds to changes

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-16-0383
Volume/Issue:
Volume 233: Issue 1
Free access
Sihan Lv Department of Endocrinology, Shanghai Tenth People’s Hospital, School of Medicine, Tongji University, Shanghai, China

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Xinchen Qiu Department of Endocrinology, Shanghai Tenth People’s Hospital, School of Medicine, Tongji University, Shanghai, China
Translational Medical Center for Stem Cell Therapy & Institute for Regenerative Medicine, Shanghai East Hospital, School of Life Sciences and Technology, Tongji University, Shanghai, China

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Jian Li Department of Endocrinology, Shanghai Tenth People’s Hospital, School of Medicine, Tongji University, Shanghai, China
Translational Medical Center for Stem Cell Therapy & Institute for Regenerative Medicine, Shanghai East Hospital, School of Life Sciences and Technology, Tongji University, Shanghai, China

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Jinye Liang Translational Medical Center for Stem Cell Therapy & Institute for Regenerative Medicine, Shanghai East Hospital, School of Life Sciences and Technology, Tongji University, Shanghai, China

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Weida Li Translational Medical Center for Stem Cell Therapy & Institute for Regenerative Medicine, Shanghai East Hospital, School of Life Sciences and Technology, Tongji University, Shanghai, China

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Chao Zhang Translational Medical Center for Stem Cell Therapy & Institute for Regenerative Medicine, Shanghai East Hospital, School of Life Sciences and Technology, Tongji University, Shanghai, China

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Zhen-Ning Zhang Translational Medical Center for Stem Cell Therapy & Institute for Regenerative Medicine, Shanghai East Hospital, School of Life Sciences and Technology, Tongji University, Shanghai, China

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Bing Luan Department of Endocrinology, Shanghai Tenth People’s Hospital, School of Medicine, Tongji University, Shanghai, China

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glucagon’s action. Glucagon stimulates PPARα activity and targets fatty acid oxidation gene expression, which is diminished in PPARα knockout mice ( Longuet et al . 2008 ). Although AMPK is implicated to mediate glucagon-induced PPARα activity, the

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-16-0649
Volume/Issue:
Volume 234: Issue 2
Free access
Sung-Soo Park Department of Biological Sciences, College of Natural Sciences, Chonnam National University, Gwangju, South Korea

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Yeon-Joo Lee Department of Biological Sciences, College of Natural Sciences, Chonnam National University, Gwangju, South Korea

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Sooyeon Song Division of Animal Science, College of Agriculture & Life Science, Chonnam National University, Gwangju, South Korea

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Boyong Kim Gwangju Center, Korea Basic Science Institute, Gwangju, South Korea

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Hyuno Kang Gwangju Center, Korea Basic Science Institute, Gwangju, South Korea

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Sejong Oh Division of Animal Science, College of Agriculture & Life Science, Chonnam National University, Gwangju, South Korea

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Eungseok Kim Department of Biological Sciences, College of Natural Sciences, Chonnam National University, Gwangju, South Korea

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( Minnich et al . 2001 ). Recent studies have shown that the hepatic functions of SREBP-1c and PPARα could be modulated by AMPK, an energy sensor that is activated by a high AMP:ATP ratio and maintains cellular energy homeostasis in part by regulating

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-17-0592
Volume/Issue:
Volume 237: Issue 2
Free access
Fengyue Wang
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Jing Yang
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Junfeng Sun
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Yanli Dong
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Hong Zhao Laboratory of Cardiovascular Internal Medicine Department, Laboratory of Cardiovascular Internal Medicine Department, First Affiliated Hospital, Harbin Medical University, 23 Youzheng Street, Nangang District, Harbin, Heilongjiang 150001, China

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Hui Shi Laboratory of Cardiovascular Internal Medicine Department, Laboratory of Cardiovascular Internal Medicine Department, First Affiliated Hospital, Harbin Medical University, 23 Youzheng Street, Nangang District, Harbin, Heilongjiang 150001, China

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Lu Fu
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-activated protein kinase (AMPK) can be activated in many situations, such as ischemia, pressure overload, and heart failure, and its activation can upregulate the expression of PGC1A ( Rowe et al . 2010 , Zaha & Young 2012 ). Both decreased PGC1A and adverse

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-14-0638
Volume/Issue:
Volume 225: Issue 2
Free access
Miski Scerif Centre for Endocrinology, Department of Endocrine Neurobiology, Division of Endocrinology, Oxford Centre for Diabetes, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK

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Tamás Füzesi Centre for Endocrinology, Department of Endocrine Neurobiology, Division of Endocrinology, Oxford Centre for Diabetes, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK

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Julia D Thomas Centre for Endocrinology, Department of Endocrine Neurobiology, Division of Endocrinology, Oxford Centre for Diabetes, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK

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Blerina Kola Centre for Endocrinology, Department of Endocrine Neurobiology, Division of Endocrinology, Oxford Centre for Diabetes, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK

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Ashley B Grossman Centre for Endocrinology, Department of Endocrine Neurobiology, Division of Endocrinology, Oxford Centre for Diabetes, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK
Centre for Endocrinology, Department of Endocrine Neurobiology, Division of Endocrinology, Oxford Centre for Diabetes, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK

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Csaba Fekete Centre for Endocrinology, Department of Endocrine Neurobiology, Division of Endocrinology, Oxford Centre for Diabetes, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK
Centre for Endocrinology, Department of Endocrine Neurobiology, Division of Endocrinology, Oxford Centre for Diabetes, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK

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Márta Korbonits Centre for Endocrinology, Department of Endocrine Neurobiology, Division of Endocrinology, Oxford Centre for Diabetes, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK

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observed during glucocorticoid excess correspond to the metabolic steps regulated by AMP-activated protein kinase (AMPK). AMPK is a regulator of cellular and systemic energy homeostasis and acts as a sensor of energy status. AMPK may be activated through

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-13-0192
Volume/Issue:
Volume 219: Issue 1
Free access
Chaoyi Zhang Key Laboratory of Bio-Resource and Eco-Environment of Ministry of Education, College of Life Sciences, Sichuan University, Chengdu, China

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Qianli Zhang Key Laboratory of Bio-Resource and Eco-Environment of Ministry of Education, College of Life Sciences, Sichuan University, Chengdu, China

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Zhihong Huang Key Laboratory of Bio-Resource and Eco-Environment of Ministry of Education, College of Life Sciences, Sichuan University, Chengdu, China

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Quan Jiang Key Laboratory of Bio-Resource and Eco-Environment of Ministry of Education, College of Life Sciences, Sichuan University, Chengdu, China

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-activated protein kinase (AMPK), a heterotrimeric enzyme complex, is the key regulator of energy metabolism in cells, which contributes to the regulation of most metabolic pathways, including glucose metabolism and lipid metabolism ( Kahn et al. 2005 ). Recent

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Research Article
DOI:
https://doi.org/10.1530/JOE-20-0077
Volume/Issue:
Volume 246: Issue 2
Restricted access