Abstract
Glucagon-like peptide-1 (GLP-1) may contribute to the decreased incretin effect characterizing type 2 diabetes. Multiple actions other than insulin secretion stimulation give to GLP-1 a highly desirable profile for an antidiabetic agent. To overcome the need for continuous infusion of the native compound, which is rapidly degraded by dimethyl-peptidyl-peptidase-IV (DPP-IV), analogues with low affinity for this protease have been developed. A second major strategy is represented by DPP-IV inhibitors that act to increase endogenous GLP-1. On the basis of the promising results in clinical trials, the incretin-based therapy may offer an useful option for diabetes management.
MeSH terms
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Diabetes Mellitus, Type 2 / drug therapy*
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Dipeptidyl Peptidase 4
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Dipeptidyl-Peptidase IV Inhibitors
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Drug Delivery Systems
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Enzyme Inhibitors / therapeutic use
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Gastric Inhibitory Polypeptide / physiology
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Glucagon-Like Peptide 1 / analogs & derivatives
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Glucagon-Like Peptide 1 / metabolism
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Glucagon-Like Peptide 1 / physiology
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Glucagon-Like Peptide 1 / therapeutic use*
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Humans
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Hypoglycemic Agents / therapeutic use
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Incretins / pharmacology
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Liraglutide
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Maleimides / therapeutic use
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Peptides / therapeutic use
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Protein Processing, Post-Translational
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Signal Transduction / drug effects
Substances
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CJC 1131
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Dipeptidyl-Peptidase IV Inhibitors
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Enzyme Inhibitors
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Hypoglycemic Agents
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Incretins
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Maleimides
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Peptides
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Gastric Inhibitory Polypeptide
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Liraglutide
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Glucagon-Like Peptide 1
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DPP4 protein, human
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Dipeptidyl Peptidase 4