This study shows that endothelial cells are the primary source of circulating FABP4 under basal conditions. Using conditional Knockout models, the authors found that endothelial-specific deletion of Fabp4 significantly reduced plasma FABP4 and impaired lipolysis-driven insulin secretion, highlighting a novel endocrine role for endothelial cells in systemic metabolic regulation.
Endothelial-derived FABP4 represents the majority of baseline circulating FABP4 and is critical for insulin secretion during lipolysis. Its absence blunts the metabolic response despite adipocyte-derived induction.
Endothelial-specific Fabp4 conditional Knockout mouse (Endo-KO), generated by crossing Fabp4^flox/flox mice with VE-cadherin-Cre mice to delete Fabp4 in endothelial cells.
Metabolism, Lipolysis, Endothelial signaling, Insulin secretion, FABP4
Conditional Knockout, Endothelial-specific deletion, VE-cadherin-Cre, Fabp4 floxed
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