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Therefore, our current study is consistent with a model where, during HFHC dietinduced metabolic dysregulation, the deletion of Dpp4 within Tie2 + cells increases the abundance of GLP-1 delivered to the systemic circulation, enabling the incretin effect, and improves oral glucose tolerance but does not affect HGP

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Glucagon-like peptide-1 (GLP-1) is an incretin hormone primarily produced by intestinal L-cells in response to nutrient intake

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