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Muraly Puttabyatappa Department of Pediatrics, University of Michigan, Ann Arbor, Michigan, USA

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Robert M Sargis Department of Medicine, University of Illinois at Chicago, Chicago, Illinois, USA

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Vasantha Padmanabhan Department of Pediatrics, University of Michigan, Ann Arbor, Michigan, USA

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Introduction Insulin resistance is a characteristic feature of many metabolic disorders, including the metabolic syndrome, type 2 diabetes mellitus (T2DM), obesity, non-alcoholic fatty liver disease (NAFLD), polycystic ovary syndrome (PCOS

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JOE-20-0044
Volume/Issue:
Volume 245: Issue 3
Free access
Nicole G Barra Department of Biochemistry and Biomedical Sciences, Department of Biochemistry and Biomedical Sciences, Farncombe Family Digestive Health Research Institute, Centre for Metabolism, Obesity and Diabetes Research, McMaster University, Hamilton, Ontario, Canada

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Fernando F Anhê Department of Biochemistry and Biomedical Sciences, Department of Biochemistry and Biomedical Sciences, Farncombe Family Digestive Health Research Institute, Centre for Metabolism, Obesity and Diabetes Research, McMaster University, Hamilton, Ontario, Canada

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Joseph F Cavallari Department of Biochemistry and Biomedical Sciences, Department of Biochemistry and Biomedical Sciences, Farncombe Family Digestive Health Research Institute, Centre for Metabolism, Obesity and Diabetes Research, McMaster University, Hamilton, Ontario, Canada

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Anita M Singh Department of Biochemistry and Biomedical Sciences, Department of Biochemistry and Biomedical Sciences, Farncombe Family Digestive Health Research Institute, Centre for Metabolism, Obesity and Diabetes Research, McMaster University, Hamilton, Ontario, Canada

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Darryl Y Chan Department of Biochemistry and Biomedical Sciences, Department of Biochemistry and Biomedical Sciences, Farncombe Family Digestive Health Research Institute, Centre for Metabolism, Obesity and Diabetes Research, McMaster University, Hamilton, Ontario, Canada

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Jonathan D Schertzer Department of Biochemistry and Biomedical Sciences, Department of Biochemistry and Biomedical Sciences, Farncombe Family Digestive Health Research Institute, Centre for Metabolism, Obesity and Diabetes Research, McMaster University, Hamilton, Ontario, Canada

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extraction from food ( Bäckhed et al. 2007 ). The gut microbiota can also influence blood glucose. Lower bacterial diversity correlates with insulin resistance and higher adiposity (reviewed in Zhu & Goodarzi 2020 ). Type 2 diabetes (T2D) is associated

Article Type:
Review Article
Collections:
Gut microbiome special collection, Top-cited articles of 2023
DOI:
https://doi.org/10.1530/JOE-21-0081
Volume/Issue:
Volume 250: Issue 2
Free access
Kok Lim Kua Stead Family Department of Pediatrics, Carver College of Medicine, University of Iowa, Iowa City, Iowa, USA

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Shanming Hu Stead Family Department of Pediatrics, Carver College of Medicine, University of Iowa, Iowa City, Iowa, USA

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Chunlin Wang Stead Family Department of Pediatrics, Carver College of Medicine, University of Iowa, Iowa City, Iowa, USA

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Jianrong Yao Stead Family Department of Pediatrics, Carver College of Medicine, University of Iowa, Iowa City, Iowa, USA

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Diana Dang Stead Family Department of Pediatrics, Carver College of Medicine, University of Iowa, Iowa City, Iowa, USA

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Alexander B Sawatzke Stead Family Department of Pediatrics, Carver College of Medicine, University of Iowa, Iowa City, Iowa, USA

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Jeffrey L Segar Stead Family Department of Pediatrics, Carver College of Medicine, University of Iowa, Iowa City, Iowa, USA

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Kai Wang Department of Biostatistics, College of Public Health, University of Iowa, Iowa City, Iowa, USA

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Andrew W Norris Stead Family Department of Pediatrics, Carver College of Medicine, University of Iowa, Iowa City, Iowa, USA
Department of Biochemistry, Carver College of Medicine, University of Iowa, Iowa City, Iowa, USA
Fraternal Order of Eagles Diabetes Research Center, University of Iowa, Iowa City, Iowa, USA

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Introduction Offspring born from pregnancy complicated by diabetes have a lifelong increased risk of insulin resistance. In humans, such offspring have a 4- to 8-fold higher risk, beyond genetic risk, to develop type 2 diabetes, metabolic

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-18-0455
Volume/Issue:
Volume 242: Issue 1
Free access
Jiean Xu State Key Laboratory of Chemical Oncogenomics, Key Laboratory of Chemical Genomics, Peking University Shenzhen Graduate School, Shenzhen, China
Vascular Biology Center, Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta University, Augusta, Georgia, USA

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Qiuhua Yang State Key Laboratory of Chemical Oncogenomics, Key Laboratory of Chemical Genomics, Peking University Shenzhen Graduate School, Shenzhen, China
Vascular Biology Center, Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta University, Augusta, Georgia, USA

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Xiaoyu Zhang State Key Laboratory of Chemical Oncogenomics, Key Laboratory of Chemical Genomics, Peking University Shenzhen Graduate School, Shenzhen, China
Vascular Biology Center, Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta University, Augusta, Georgia, USA

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Zhiping Liu State Key Laboratory of Chemical Oncogenomics, Key Laboratory of Chemical Genomics, Peking University Shenzhen Graduate School, Shenzhen, China
Vascular Biology Center, Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta University, Augusta, Georgia, USA

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Yapeng Cao State Key Laboratory of Chemical Oncogenomics, Key Laboratory of Chemical Genomics, Peking University Shenzhen Graduate School, Shenzhen, China
Vascular Biology Center, Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta University, Augusta, Georgia, USA

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Lina Wang State Key Laboratory of Chemical Oncogenomics, Key Laboratory of Chemical Genomics, Peking University Shenzhen Graduate School, Shenzhen, China
Vascular Biology Center, Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta University, Augusta, Georgia, USA

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Yaqi Zhou State Key Laboratory of Chemical Oncogenomics, Key Laboratory of Chemical Genomics, Peking University Shenzhen Graduate School, Shenzhen, China
Vascular Biology Center, Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta University, Augusta, Georgia, USA

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Xianqiu Zeng State Key Laboratory of Chemical Oncogenomics, Key Laboratory of Chemical Genomics, Peking University Shenzhen Graduate School, Shenzhen, China
Vascular Biology Center, Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta University, Augusta, Georgia, USA

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Qian Ma State Key Laboratory of Chemical Oncogenomics, Key Laboratory of Chemical Genomics, Peking University Shenzhen Graduate School, Shenzhen, China
Vascular Biology Center, Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta University, Augusta, Georgia, USA

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Yiming Xu Vascular Biology Center, Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta University, Augusta, Georgia, USA
School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, China

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Yong Wang Vascular Biology Center, Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta University, Augusta, Georgia, USA
College of Basic Medicine, Chengdu University of Traditional Chinese Medicine, Chengdu, China

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Lei Huang Department of Cardiovascular Surgery, Peking University Shenzhen Hospital, Shenzhen, China

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Zhen Han Department of Cardiovascular Surgery, Peking University Shenzhen Hospital, Shenzhen, China

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Tao Wang Department of Cardiovascular Surgery, Peking University Shenzhen Hospital, Shenzhen, China

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David Stepp Vascular Biology Center, Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta University, Augusta, Georgia, USA

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Zsolt Bagi Department of Physiology, Medical College of Georgia, Augusta University, Augusta, Georgia, USA

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Chaodong Wu Department of Nutrition and Food Science, Texas A&M University, College Station, Texas, USA

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Mei Hong State Key Laboratory of Chemical Oncogenomics, Key Laboratory of Chemical Genomics, Peking University Shenzhen Graduate School, Shenzhen, China

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Yuqing Huo Vascular Biology Center, Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta University, Augusta, Georgia, USA

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resistance-associated metabolic perturbations. Accumulating evidence highlights a critical role for adenosine signaling in the development of insulin resistance ( Antonioli et al. 2015 , Pardo et al. 2017 ). Adenosine signaling is also closely

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-19-0126
Volume/Issue:
Volume 242: Issue 2
Free access
Gencer Sancar German Center for Diabetes Research, Neuherberg, Germany
Department of Internal Medicine IV, Division of Diabetology, Endocrinology and Nephrology, Eberhard-Karls University of Tübingen, Tübingen, Germany
Institute for Diabetes Research and Metabolic Diseases, Helmholtz Center Munich, Eberhard-Karls University of Tübingen, Tübingen, Germany

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Andreas L Birkenfeld German Center for Diabetes Research, Neuherberg, Germany
Department of Internal Medicine IV, Division of Diabetology, Endocrinology and Nephrology, Eberhard-Karls University of Tübingen, Tübingen, Germany
Institute for Diabetes Research and Metabolic Diseases, Helmholtz Center Munich, Eberhard-Karls University of Tübingen, Tübingen, Germany

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metabolic disturbances is insulin resistance, which is a condition in which the body's cells become resistant to the effects of insulin, leading to impaired glucose and lipid homeostasis. Adipose tissue dysfunction plays a crucial role in the development of

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JOE-24-0115
Volume/Issue:
Volume 262: Issue 3
Open access
Sandra Pereira Department of Physiology, Department of Medicine, Toronto General Research Institute, Banting and Best Diabetes Centre, Institute of Medical Science, School of Pharmacy, University of Toronto, Medical Sciences Building, 1 King's College Circle, Toronto, Ontario, Canada M5S 1A8

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Anu Shah Department of Physiology, Department of Medicine, Toronto General Research Institute, Banting and Best Diabetes Centre, Institute of Medical Science, School of Pharmacy, University of Toronto, Medical Sciences Building, 1 King's College Circle, Toronto, Ontario, Canada M5S 1A8

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I George Fantus Department of Physiology, Department of Medicine, Toronto General Research Institute, Banting and Best Diabetes Centre, Institute of Medical Science, School of Pharmacy, University of Toronto, Medical Sciences Building, 1 King's College Circle, Toronto, Ontario, Canada M5S 1A8
Department of Physiology, Department of Medicine, Toronto General Research Institute, Banting and Best Diabetes Centre, Institute of Medical Science, School of Pharmacy, University of Toronto, Medical Sciences Building, 1 King's College Circle, Toronto, Ontario, Canada M5S 1A8
Department of Physiology, Department of Medicine, Toronto General Research Institute, Banting and Best Diabetes Centre, Institute of Medical Science, School of Pharmacy, University of Toronto, Medical Sciences Building, 1 King's College Circle, Toronto, Ontario, Canada M5S 1A8
Department of Physiology, Department of Medicine, Toronto General Research Institute, Banting and Best Diabetes Centre, Institute of Medical Science, School of Pharmacy, University of Toronto, Medical Sciences Building, 1 King's College Circle, Toronto, Ontario, Canada M5S 1A8
Department of Physiology, Department of Medicine, Toronto General Research Institute, Banting and Best Diabetes Centre, Institute of Medical Science, School of Pharmacy, University of Toronto, Medical Sciences Building, 1 King's College Circle, Toronto, Ontario, Canada M5S 1A8

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Jamie W Joseph Department of Physiology, Department of Medicine, Toronto General Research Institute, Banting and Best Diabetes Centre, Institute of Medical Science, School of Pharmacy, University of Toronto, Medical Sciences Building, 1 King's College Circle, Toronto, Ontario, Canada M5S 1A8

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Adria Giacca Department of Physiology, Department of Medicine, Toronto General Research Institute, Banting and Best Diabetes Centre, Institute of Medical Science, School of Pharmacy, University of Toronto, Medical Sciences Building, 1 King's College Circle, Toronto, Ontario, Canada M5S 1A8
Department of Physiology, Department of Medicine, Toronto General Research Institute, Banting and Best Diabetes Centre, Institute of Medical Science, School of Pharmacy, University of Toronto, Medical Sciences Building, 1 King's College Circle, Toronto, Ontario, Canada M5S 1A8
Department of Physiology, Department of Medicine, Toronto General Research Institute, Banting and Best Diabetes Centre, Institute of Medical Science, School of Pharmacy, University of Toronto, Medical Sciences Building, 1 King's College Circle, Toronto, Ontario, Canada M5S 1A8
Department of Physiology, Department of Medicine, Toronto General Research Institute, Banting and Best Diabetes Centre, Institute of Medical Science, School of Pharmacy, University of Toronto, Medical Sciences Building, 1 King's College Circle, Toronto, Ontario, Canada M5S 1A8

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Introduction Obesity is associated with elevated circulating free fatty acids (FFAs) and FFAs cause insulin resistance ( Lewis et al . 2002 , Xiao et al . 2008 ). FFAs induce oxidative stress ( Nakamura et al . 2009 , Yuzefovych et al . 2010

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-14-0676
Volume/Issue:
Volume 225: Issue 1
Free access
Nigel Turner Department of Pharmacology, School of Medical Sciences, Diabetes and Obesity Division, St Vincent's Clinical School, Department of Physiology, University of New South Wales, Sydney, New South Wales, Australia
Department of Pharmacology, School of Medical Sciences, Diabetes and Obesity Division, St Vincent's Clinical School, Department of Physiology, University of New South Wales, Sydney, New South Wales, Australia

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Gregory J Cooney Department of Pharmacology, School of Medical Sciences, Diabetes and Obesity Division, St Vincent's Clinical School, Department of Physiology, University of New South Wales, Sydney, New South Wales, Australia
Department of Pharmacology, School of Medical Sciences, Diabetes and Obesity Division, St Vincent's Clinical School, Department of Physiology, University of New South Wales, Sydney, New South Wales, Australia

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Edward W Kraegen Department of Pharmacology, School of Medical Sciences, Diabetes and Obesity Division, St Vincent's Clinical School, Department of Physiology, University of New South Wales, Sydney, New South Wales, Australia
Department of Pharmacology, School of Medical Sciences, Diabetes and Obesity Division, St Vincent's Clinical School, Department of Physiology, University of New South Wales, Sydney, New South Wales, Australia

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Clinton R Bruce Department of Pharmacology, School of Medical Sciences, Diabetes and Obesity Division, St Vincent's Clinical School, Department of Physiology, University of New South Wales, Sydney, New South Wales, Australia

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(obesity) and reduced insulin action (insulin resistance) in muscle, this article will deal with FAs as an alternative energy substrate to glucose, the relevance of this substrate competition to overall energy expenditure and an assessment of the various

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JOE-13-0397
Volume/Issue:
Volume 220: Issue 2
Free access
Lidong Zhai Division of Molecular and Cellular Pathology, Veterans Affairs Medical Center, Department of Pathology, The University of Alabama at Birmingham, 1670 University Boulevard, Birmingham, Alabama 35294-0019, USA

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Joseph L Messina Division of Molecular and Cellular Pathology, Veterans Affairs Medical Center, Department of Pathology, The University of Alabama at Birmingham, 1670 University Boulevard, Birmingham, Alabama 35294-0019, USA
Division of Molecular and Cellular Pathology, Veterans Affairs Medical Center, Department of Pathology, The University of Alabama at Birmingham, 1670 University Boulevard, Birmingham, Alabama 35294-0019, USA

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Introduction Acute insulin resistance is common following trauma, hemorrhage, sepsis, burn, and critical illness ( Ikezu et al . 1997 , Carter 1998 , Van den Berghe et al . 2001 , Cree & Wolfe 2008 ). Chronic insulin resistant states, such as

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-09-0269
Volume/Issue:
Volume 203: Issue 3
Free access
Mohamed Asrih Service of Endocrinology, Diabetes, Hypertension and Nutrition, Geneva University Hospital, Rue Gabrielle‐Perret‐Gentil 4, 1211 Genève 14, Switzerland

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François R Jornayvaz Service of Endocrinology, Diabetes, Hypertension and Nutrition, Geneva University Hospital, Rue Gabrielle‐Perret‐Gentil 4, 1211 Genève 14, Switzerland

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, insulin resistance, hypertension, and dyslipidemia, suggesting that NAFLD might be considered as the liver manifestation of the metabolic syndrome ( Marchesini et al . 2001 , Adams et al . 2005 ). The metabolic syndrome is a leading cause of mortality

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JOE-13-0201
Volume/Issue:
Volume 218: Issue 3
Free access
Sergio Di Meo Dipartimento di Biologia, Università di Napoli ‘Federico II’, Napoli, Italy

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Susanna Iossa Dipartimento di Biologia, Università di Napoli ‘Federico II’, Napoli, Italy

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Paola Venditti Dipartimento di Biologia, Università di Napoli ‘Federico II’, Napoli, Italy

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increased the most in obese people, compared with lean ones, is type 2 diabetes mellitus (T2DM), a condition resulting from the metabolic changes associated with excess fat. A pivotal role in T2DM development is played by insulin resistance (IR) that is

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JOE-17-0186
Volume/Issue:
Volume 234: Issue 3
Free access