0175 : Phenotypic remodeling of perivascular adipose tissue in a rat model of metabolic syndrome: vascular consequences and beneficial impact of exercise training

Aim This study was designed to evaluate the impact of high fat and high sucrose diet (HFS) on perivascular adipose tissue (PVAT) and its consequence on vascular function. Whether exercise training was able to counteract this alterations has been investigated as a potential therapeutic strategy. Methods Rats were fed with standard (Ctrl rats) or HFS diet (HFS rats) for 15 weeks. After 6 weeks, HFS rats were randomly assigned into 2 groups: sedentary and trained group (HFS-Ex). PVAT remodeling was assessed by a proteome profiler, histological and biochemical assays. The impact of PVAT secretion on vascular function was assessed on isolated aortic rings incubated or not with PVAT secretum. Results and discussion We reported increased PVAT mass in HFS rats associated with increase in both white to brown adipocytes proportion and uncoupling protein 1 level. Despite no major effect of HFS diet on PVAT adipokines profile was reported, adiponectin level and secretion were reduced in PVAT of HFS rats. As a potential consequence, we observed a marked endothelial dysfunction in Ctrl aortic rings incubated with PVAT secretum of HFS rats. The use of a non-specific antioxidant (N-Acetyl cysteine) in the organ bath blunted the deleterious effect of HFS secretum on endothelial function, suggesting a redox-dependent mechanism in this phenomenon. Exercise training in HFS rats normalized PVAT mass but has no effect on the browning process. However, this strategy was able to normalize adiponectin level in PVAT of HFS rats and finally abolished the detrimental effect of its secretion on endothelial function. Conclusion Diet-induced metabolic syndrome leads to PVAT remodeling inducing deleterious vasoactives properties. The ability of exercise training to modulate this phenomenon could be considered as a good strategy to counteract the potential role of PVAT in the development of chronic vascular dysfunction in metabolic syndrome disease. The author hereby declares no conflict of interest