The aim of this study was to evaluate the preventive and therapeutic effect of coffee consumption on metabolic and molecular aspects of adipose tissue (AT) remodeling in a high‐fat diet‐induced obesity mice. Our hypothesis is that coffee consumption mitigates brown adipose tissue (BAT) whitening and prevent obesity related comorbidities. 50 male mice of 90 days of the C57BL6 lineage divided into 3 groups: Control (C); High‐fat (HF) and prevention 1% w/w coffee (HF‐CP). After 10 weeks, the HF group gave rise to the treatment 1% w/w coffee group (HF‐CT), totaling 4 different groups for another 4 weeks, totaling 14 weeks of experiment. The HF‐CP group has lower body mass than the high fat (HF) group (‐8%, p < 0.05), better AT distribution, with smaller adipocytes and smaller mean sectional area (p<0.05). Both groups that received coffee associated with a high‐fat diet (HF‐CP and HF‐CT) improved glucose metabolism when compared to the HF group, the glucose tolerance test in the HF‐CP group was similar to the C. Coffee consumption prevented hyperinsulinemia and hyperleptinemia in the HF‐CP group, this group did not develop insulin resistance and in the group that consumed coffee after induction of obesity (HF‐CT) the hyperinsulinemia was attenuated. The plasma concentration of IL‐6 was reduced (p<0.05) in HF‐CP and HF‐CT when compared to the HF group. The immunofluorescence expression of UCP‐1was more intense in BAT of HF‐CP compared to others groups. Thermogenesis and mitochondrial biogenesis in BAT were higher with increased gene expression of UCP‐1, PPARγ, PRDM16, PCG1α, Rβ3A, OPA‐1in HF‐CP. Coffee has better effects when consumed preventively with better AT remodeling, with maintenance of the brown phenotype, thermogenic activity in BAT. Furthermore, coffee consumption was able to attenuate body mass gain, improve glucose and leptin homeostasis. When consumed after obesity induction, as a treatment, it was not as effective as prevention, however, there was also better BAT remodeling with attenuation of lightening, greater expression of thermogenic genes and reversal of hyperinsulinemia.