Abstract
Insulin resistance is closely associated with obesity and type 2 diabetes. Although the mechanisms of insulin resistance are not fully elucidated, recent studies suggest that a complex interaction between inflammation, endoplasmic reticulum stress, oxidative stress, mitochondrial dysfunction and autophagy dysregulation plays an important role in insulin resistance. The stress-activated c-Jun N-terminal kinase (JNK) has been increasingly recognized as a central mediator of insulin resistance. JNK mediates many of the effects of stress on insulin resistance through inhibitory phosphorylation of insulin receptor substrate, and suppression of the JNK pathway has been shown to improve insulin resistance and glucose tolerance. Therefore JNK may serve as a crucial link between stress and metabolic diseases as well as a promising therapeutic target. This review focuses on recent findings that support a critical role for JNK in the development of insulin resistance associated with inflammation, endoplasmic reticulum stress, oxidative stress and mitochondrial dysfunction. JNK regulation of autophagy and its implications in insulin resistance also will be discussed.
Keywords: Autophagy, endoplasmic reticulum stress, inflammation, insulin resistance, JNK, mitochondrial dysfunction, obesity, oxidative stress.
Current Diabetes Reviews
Title:Emerging Role of JNK in Insulin Resistance
Volume: 9 Issue: 5
Author(s): Hongliang Li and Xichun Yu
Affiliation:
Keywords: Autophagy, endoplasmic reticulum stress, inflammation, insulin resistance, JNK, mitochondrial dysfunction, obesity, oxidative stress.
Abstract: Insulin resistance is closely associated with obesity and type 2 diabetes. Although the mechanisms of insulin resistance are not fully elucidated, recent studies suggest that a complex interaction between inflammation, endoplasmic reticulum stress, oxidative stress, mitochondrial dysfunction and autophagy dysregulation plays an important role in insulin resistance. The stress-activated c-Jun N-terminal kinase (JNK) has been increasingly recognized as a central mediator of insulin resistance. JNK mediates many of the effects of stress on insulin resistance through inhibitory phosphorylation of insulin receptor substrate, and suppression of the JNK pathway has been shown to improve insulin resistance and glucose tolerance. Therefore JNK may serve as a crucial link between stress and metabolic diseases as well as a promising therapeutic target. This review focuses on recent findings that support a critical role for JNK in the development of insulin resistance associated with inflammation, endoplasmic reticulum stress, oxidative stress and mitochondrial dysfunction. JNK regulation of autophagy and its implications in insulin resistance also will be discussed.
Export Options
About this article
Cite this article as:
Li Hongliang and Yu Xichun, Emerging Role of JNK in Insulin Resistance, Current Diabetes Reviews 2013; 9 (5) . https://dx.doi.org/10.2174/15733998113099990074
DOI https://dx.doi.org/10.2174/15733998113099990074 |
Print ISSN 1573-3998 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6417 |
- Author Guidelines
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
- Announcements
Related Articles
-
MicroRNA Polymorphisms, MicroRNA Pharmacogenomics and Cancer Susceptibility
Current Pharmacogenomics and Personalized Medicine Novel Approaches to Study the Involvement of α7-nAChR in Human Diseases
Current Drug Targets Opioid-modulating Peptides: Mechanisms of Action
Current Topics in Medicinal Chemistry Channel-Like Functions of the 18-kDa Translocator Protein (TSPO): Regulation of Apoptosis and Steroidogenesis as Part of the Host-Defense Response
Current Pharmaceutical Design Patent Selections
Recent Patents on DNA & Gene Sequences Stress Hormone-Mediated DNA Damage Response -- Implications for Cellular Senescence and Tumour Progression
Current Drug Targets The Metabolite Trimethylamine-N-Oxide is an Emergent Biomarker of Human Health
Current Medicinal Chemistry The Role of α7 Nicotinic Acetylcholine Receptors and α7-Specific Antibodies in Neuroinflammation Related to Alzheimer Disease
Current Pharmaceutical Design Assessing Combinations of Cytotoxic Agents Using Leukemia Cell Lines
Current Drug Targets Biochemical, Molecular and Epigenetic Mechanisms of Valproic Acid Neuroprotection
Current Molecular Pharmacology Human Papillomavirus E7 Oncoprotein Promotes Proliferation and Migration through the Transcription Factor E2F1 in Cervical Cancer Cells
Anti-Cancer Agents in Medicinal Chemistry Modulation of Ornithine Decarboxylase Activity by Phenolics Based Structurally Related Compounds Synthesized on Steroidal and Non-Steroidal Skeleton and their Radical Scavenging Action
Current Bioactive Compounds Replicative Oncolytic Herpes Simplex Viruses in Combination Cancer Therapies
Current Gene Therapy Caspase-8 as a Regulator of Tumor Cell Motility
Current Molecular Medicine Removing Protein Aggregates: The Role of Proteolysis in Neurodegeneration
Current Medicinal Chemistry Targeting Translation for Treatment of Cancer - A Novel Role for IRES?
Current Cancer Drug Targets Effect of Genetic Polymorphisms (SNPs) in CHRNA7 Gene on Response to Acetylcholinesterase Inhibitors (AChEI) in Patients with Alzheimer’s Disease
Current Drug Targets DNA Intercalators in Cancer Therapy: Organic and Inorganic Drugs and Their Spectroscopic Tools of Analysis
Mini-Reviews in Medicinal Chemistry Voltage-Gated Calcium Channels as Targets for the Treatment of Chronic Pain
Current Drug Targets - CNS & Neurological Disorders <i>Uncaria tomentosa</i> (Willd. ex Schult.): Focus on Nutraceutical Aspects
Current Bioactive Compounds