Glucose transport in fat cells results in accumulation of triglycerides in lipid droplets and is regulated by insulin. When a fat tissue become insulin-resistant, glucose transport into the cells is impaired and results in Type 2 diabetes. The lipid droplets accumulation is part of the adipogenesis differentiation and metabolism. In the current study, we monitored the adipogenesis of 3T3-L1 cultured cells in high and low glucose concentrations, while the cells were exposed to different substrate rigidity and tensile deformation. We have mapped, under light microscopy, the areas of cell differentiation over time, using a new matrix modelling method. Furthermore, phase contrast images were taken along the adipogenesis process and were analyzed by a MATLAB algorithm. The algorithm follows cell differentiation (cell size and morphology and nucleus size) and lipid accumulation (number of lipid droplets per cell and their radius). Complementary, we analyzed by immunofluorescence (IF) the molecular expression of PPARγ, a transcription factor, along with DNA staining by DAPI and Lamin A/C for the nucleus organization. The results indicate that substrate tensile strains delivered to adipocytes accelerate their lipid production.