The transplantation of adipose tissues in dorsal area failed to induce comparable leukocyte adhesion to those induced by contralateral femoral artery transplantation, there may be a distinct and strong pro-inflammatory mechanisms between adipose Orotic acid 6-Carboxyuracil tissue and vasculature. As previously reported, high-fat diet induces insulin resistance and various inflammatory conditions in adipose tissues. In our study, SQ was more sensitive to enhance high-fat-triggered leukocyte adhesion when compared to VIC suggesting that the inflammatory status of SQ adipose tissues may contribute to the systemic inflammation under diet-induced obesity. The accumulation of M1 macrophages and activated monocytes were prominent in VIS as compared to SQ adipose tissues, which were further enhanced by high-fat diet. We also documented an involvement of DCs in adipose tissue inflammation. Recently, free fatty acid was shown to recruit DCs from bone marrow to adipose tissues via Toll-like receptor 2/4, while another study reported that adipose tissue is one of the main source of DCs in the body. Therefore, DCs may play a major role in adipose tissue inflammation in close coordination with macrophages in dyslipidemia. Our data are consistent with these reports and confirm the importance of monocytes, macrophages and DCs accumulated in adipose tissues to regulate local inflammation. These findings extend current understanding of relationship between adipose tissue and vasculature in the context of metabolic syndrome and atherosclerosis. In conclusion, adipose tissue transplantation induced Nobiletin production of inflammatory cytokines and chemokines, resulting in leukocyte adhesion. HF intake enhanced adipose inflammation, including an increase in inflammatory molecules and accumulation of inflammatory cells such as DCs in adipose tissue. Our findings suggest that inflammation caused by adipose tissue directly induces vascular inflammation. Additional studies of the mechanisms that link adipocyte inflammation to vascular inflammation may shed new light on the complex mechanism of atherosclerosis.