Key result
Diet-induced obesity in mice did not impair endothelial regeneration following mechanical injury compared with chow-fed controls, despite the induction of an adverse metabolic phenotype.
Why the study?
Does diet-induced obesity impair endothelial regeneration following mechanical injury in mice?
Does diet-induced obesity impair endothelial regeneration following mechanical injury in mice?
In a mouse model, diet-induced obesity did not impair endothelial regeneration after mechanical injury, suggesting compensatory mechanisms preserve endothelial repair despite metabolic dysregulation.
Preserved endothelial repair in obese mice cautions against assuming defective regeneration drives CVD; leaves open compensatory mechanisms for targeted human studies.
INTRODUCTION: Preservation of structural integrity of the endothelial monolayer and maintenance of endothelial cell function are of critical importance in preventing arterial thrombosis, restenosis and atherosclerosis. Obesity has been intimately linked with endothelial dysfunction, and reports of reduced abundance and functional impairment of circulating progenitor cells in obesity have led to the suggestion that defective endothelial repair contributes to obesity-related cardiovascular disease. METHODS: C57BL/6 mice were fed a high-fat diet for either 3 or 6 months to induce obesity; metabolic phenotyping was then carried out before femoral artery wire injury was performed. Endothelial regeneration was then quantified. Mononuclear cells and myeloid angiogenic cells were cultured and characterized for pro-angiogenic properties. RESULTS: No impairment of endothelial regeneration following mechanical endothelial injury in diet-induced obese mice when compared with chow-fed controls was observed, despite the induction of an adverse metabolic phenotype characterized by glucose intolerance and insulin resistance. Dietary-obese mice had increased numbers of circulating myeloid angiogenic cells, which retained normal functional properties including intact paracrine angiogenic effects. CONCLUSION: Preserved endothelial regeneration despite metabolic dysregulation in dietary obese mice suggests that compensatory mechanisms mitigate the deleterious influence of insulin resistance on endothelial repair in obesity.
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Rashid et al. (2018) studied Diet-induced obesity. High-fat diet vs. Chow-fed controls was evaluated on Endothelial regeneration following mechanical endothelial injury. Diet-induced obesity in mice did not impair endothelial regeneration following mechanical injury compared with chow-fed controls, despite the induction of an adverse metabolic phenotype.
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