DiabetesJul 24, 2026

GIP Quickly Reduces Muscle Blood Flow Increases Caused by Insulin and GLP-1

GLP-1 Therapies Weekly Brief ↗PubMed ↗DOI ↗

Updated Jul 25, 2026

Abstract

GIP does not increase muscle perfusion but may antagonize insulin- and GLP-1-mediated microvascular recruitment.

GIP receptors are present in the blood vessel lining of skeletal muscle.
GIP may interact with insulin and GLP-1 signaling pathways.
An imbalance involving angiotensin II type 1 receptor and endothelin-1/nitric oxide may underlie GIP's effects.
GIP acts as a conditional regulator of microvascular perfusion in skeletal muscle.

Simplified

Skeletal muscle microvasculature is essential for nutrient delivery and metabolic regulation, but the vascular actions of glucose-dependent insulinotropic polypeptide (GIP) in muscle are unknown. We investigated whether GIP regulates skeletal muscle microvascular perfusion and interacts with insulin and GLP-1 signaling. GIP receptors are expressed in vascular endothelium, yet GIP alone does not increase muscle perfusion and instead antagonizes insulin- and GLP-1-mediated microvascular recruitment via possibly angiotensin II type 1 receptor-dependent endothelin-1/nitric oxide imbalance. GIP acts as a conditional regulator of skeletal muscle microvascular perfusion, revealing a novel mechanism of tissue-specific incretin regulation of nutrient partitioning.

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GIP Quickly Reduces Muscle Blood Flow Increases Caused by Insulin and GLP-1

Abstract

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