This work was focused on the effect of (-)-epicatechin (EC), a flavonoid highly represented in human diet, on fat pads changes induced by high-fat (HF) diet. C57BL/6 male mice were divided into 4 groups receiving: control diet (10% calories from fat) (C), control diet + 20 mg EC/kg body weight (BW) (CE), HF diet (60% of calories from fat) (HF) and HF diet + 20 mg EC/kg BW (HFE) for 15 w. Food, caloric intake and body weight were evaluated throughout the treatment. HF fed groups showed ~32% lower food intake than control diet fed groups. Therefore, caloric intake was not statistically different among the experimental groups (14±1 kcal/day/mice). However, the final increase in BW was higher in animals receiving HF diet, independently of the EC supplementation. Plasma glucose, triglycerides, HDL and LDL cholesterol, ALT, GPT and GOT were measured, and plasma glucose was found statistically different in HF group respect to C group. Different fat pads were studied: perirenal (PrAT), epidydimal (EAT), mesenteric (MAT) and aortic  perivascular (aPvAT) adipose tissue. HF diet induced significant expansion in the white adipose tissue pads: (47%, 55%, and 84% for PrAT, EAT, and MAT pads, respectively, p˂0.05). Inflammatory markers (IL-6 and iNOS expression) and oxidative-related modifications (gp91phox expression and MDA content) increased in association with the expansion degree. Adipocyte size was not different in HF respect to C group. In rodents, aPvAT has the typical characteristics of brown adipose tissue. HF diet induced expansion of aPvAT expressed as area/media layer thickness (C=10242±802 and HF= 17493±823 􀀀m2/􀀀m, p˂0.05). The number of adipocytes/area was significantly lower in HF respect to C group (C= 79±4, HF=49±3, p˂0.05) indicating an increase in aPvAT adipocyte size induced by HF diet. Histological observations showed changes in vacuolization pattern suggesting a shift to white adipocyte phenotype. All the observed changes in aPvAT were attenuated by EC presence in the diet. These results were confirmed by the expression of UCP-1, a marker of brown adipose tissue, measured by immunohistochemistry (C= 67±2, HF=16±2, CE= 68±3, HFE=50±3, p˂0.05 C vs HF and HF vs HFE). Taken as a whole, these results suggest that under our experimental conditions high fat diet lead to the expansion of all the white fat pads studied essentially associated to hyperplasia, with limited metabolic changes. On the contrary, aPvAT showed expansion associated to hypertrophy with signs of transition to white phenotype that was partially attenuated by the presence of EC in the diet. Considering that aPvAT dysfunction has been linked to atherosclerosis and may contribute to hypertension, this effect of EC should be explored in depth to provide an alternative nutritional strategy to avoid the progression of vascular dysfunction in obesity. Supported by PIP 11220170100585C (MG), UBACyT  20020160100132BA (CGF); the Packer-Wentz endowment 2017 (CGF).