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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
A novel paradigm for heart failure with preserved ejection fraction: comorbidities drive myocardial dysfunction and remodeling through coronary microvascular endothelial inflammation
The CDC estimates that nearly 42% of the U.S
Intestinal neuroendocrine cells and goblet cells are mediators of IL-17A-amplified epithelial IL-17C production in human inflammatory bowel disease
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