Abstract
In Type 2 diabetes the body either produces too little insulin, or does not respond well to it. Current pharmacological treatments, which are less than optimal, either target defective insulin secretion (sulfonylureas, glinides) or insulin resistance (metformin, thiazolidinediones). Exciting new research is now helping us to understand novel pathways that may contribute to defective insulin secretion as well as decreased response to insulin. Such pathways may explain the development of diabetes and associated complications (atherosclerosis and diabetic nephropathy). Understanding the way a cell metabolises glucose may be the key to understanding how cells secrete insulin and respond to it.
MeSH terms
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Anti-Inflammatory Agents / therapeutic use
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Antioxidants / therapeutic use
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Cytokines / antagonists & inhibitors
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Cytokines / physiology
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Diabetes Mellitus, Type 2 / epidemiology
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Diabetes Mellitus, Type 2 / etiology*
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Diabetes Mellitus, Type 2 / metabolism
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Diabetes Mellitus, Type 2 / physiopathology
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Energy Metabolism
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Fatty Acids, Nonesterified / metabolism
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Gene Expression Regulation / physiology
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Glucose / metabolism
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Humans
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Hypoglycemic Agents / classification
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Hypoglycemic Agents / pharmacology
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Hypoglycemic Agents / therapeutic use
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I-kappa B Kinase
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Inflammation / complications*
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Insulin / physiology
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Insulin Resistance
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JNK Mitogen-Activated Protein Kinases / antagonists & inhibitors
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Mitochondria / physiology
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Models, Biological
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Muscle, Skeletal / metabolism
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NF-kappa B / metabolism
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Oxidative Stress* / drug effects
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Oxidative Stress* / immunology
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Oxidative Stress* / physiology
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Protein Serine-Threonine Kinases / antagonists & inhibitors
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Reactive Oxygen Species / metabolism
Substances
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Anti-Inflammatory Agents
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Antioxidants
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Cytokines
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Fatty Acids, Nonesterified
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Hypoglycemic Agents
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Insulin
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NF-kappa B
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Reactive Oxygen Species
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Protein Serine-Threonine Kinases
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CHUK protein, human
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I-kappa B Kinase
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IKBKB protein, human
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IKBKE protein, human
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JNK Mitogen-Activated Protein Kinases
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Glucose