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(54) found that administering GIPR antagonist to healthy humans reduced postprandial insulin secretion and increased glucose excursions more than administering GLP-1R antagonist (GLP-1RA), indicating that endogenous GIP may play a more significant role in stimulating insulin secretion and reducing postprandial plasma glucose excursions compared to endogenous GLP-1

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Since FM is a multifactorial disease, in which proinflammatory factors and central sensitization are currently considered to play a major role [14, 20], treatment should include pharmacological and non-pharmacological approaches