Abstract
This review outlines the physiology of protein tyrosine phosphatase 1B (PTP1B) and its potential involvement in the states of insulin resistance that characterizes both obesity and type 2 diabetes. The primary focus of this review is upon the elucidation of the role and control of PTP1B enzyme activity in obesity and type 2 diabetes. Furthermore, since selectivity and cell permeability are the two most important requirements for the development of successful PTP1B inhibitors, recent progress in finding compounds meeting these criteria are discussed.
MeSH terms
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Animals
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Anti-Obesity Agents / pharmacology
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Anti-Obesity Agents / therapeutic use*
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Enzyme Inhibitors / pharmacology
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Enzyme Inhibitors / therapeutic use*
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Humans
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Hypoglycemic Agents / pharmacology
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Hypoglycemic Agents / therapeutic use*
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Insulin / physiology
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Mice
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Mice, Knockout
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Obesity / drug therapy*
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Oligonucleotides, Antisense / pharmacology
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Oligonucleotides, Antisense / therapeutic use
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Protein Tyrosine Phosphatase, Non-Receptor Type 1
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Protein Tyrosine Phosphatases / antagonists & inhibitors*
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Protein Tyrosine Phosphatases / genetics
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Protein Tyrosine Phosphatases / physiology
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Signal Transduction / drug effects
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Signal Transduction / physiology
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Substrate Specificity
Substances
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Anti-Obesity Agents
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Enzyme Inhibitors
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Hypoglycemic Agents
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Insulin
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Oligonucleotides, Antisense
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PTPN1 protein, human
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Protein Tyrosine Phosphatase, Non-Receptor Type 1
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Protein Tyrosine Phosphatases
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Ptpn1 protein, mouse