Abstract
The multifactorial nature of the pathogenesis of T2DM provides an opportunity to combine treatments that act upon different mechanisms. In addition to improving insulin resistance and pancreatic β-cell dysfunction, the GLP-1 agonists and DPP-4 inhibitors improve the impaired incretin response, as well as increase insulin secretion and reduce glucagon secretion, both in a glucose-dependent manner. As a result of these multiple actions, the GLP-1 agonists and DPP-4 inhibitors lower both fasting and postprandial glucose levels. The effects of GLP-1 agonists tend to be greater, probably because they produce pharmacologic levels of GLP-1 compared to physiologic levels with the DPP-4 inhibitors. Another difference is that unlike the DPP-4 inhibitors, the GLP-1 agonists also slow gastric emptying and promote satiety.
MeSH terms
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Adamantane / analogs & derivatives
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Adamantane / therapeutic use
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Aged
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Blood Glucose
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Diabetes Mellitus, Type 2 / drug therapy*
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Diabetes Mellitus, Type 2 / physiopathology*
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Dipeptides / therapeutic use
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Exenatide
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Female
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Glucagon / metabolism
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Glucagon / therapeutic use
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Glucagon-Like Peptide 1 / analogs & derivatives
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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 / therapeutic use*
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Insulin-Secreting Cells / physiology
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Liraglutide
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Male
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Metformin / therapeutic use
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Middle Aged
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Peptides / therapeutic use
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Pyrazines / therapeutic use
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Severity of Illness Index
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Sitagliptin Phosphate
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Time Factors
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Triazoles / therapeutic use
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Venoms / therapeutic use
Substances
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Blood Glucose
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Dipeptides
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Hypoglycemic Agents
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Incretins
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Peptides
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Pyrazines
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Triazoles
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Venoms
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Liraglutide
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Glucagon-Like Peptide 1
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Glucagon
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Metformin
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saxagliptin
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Exenatide
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Adamantane
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Sitagliptin Phosphate