Obesity is defined as an excessive accumulation of adipose tissue within the human body. The global prevalence of obesity has seen a marked increase, and our country is no exception to this trend. The pathogenesis of obesity is intricately linked to the consumption of glucose, a phenomenon in which glucose absorption plays a pivotal role via the enterocytes of the intestinal lining. In individuals with obesity, both dietary and blood glucose levels are elevated, thereby intensifying the exposure of enterocyte cells to glucose. This thesis results delved into the interactions between high-glucose-associated zinc metabolism and zinc-dependent glucose metabolism within enterocyte cells. Results revealed a correlation between elevated glucose concentrations and reduced zinc levels within the cells, coupled with the regulation of mRNA levels on zinc transporters. Additionally, observed a reduction in cellular 2-deoxy-glucose uptake upon zinc treatment. Also, indicated that zinc treatments, whether administered to the basolateral or both apical and basolateral sides of the cells, led to the regulation of mRNA levels for glucose transporters, compared to control groups. Remarkably, also observed that specific treatments involving zinc on the polarized sides of Caco-2 cells increased the efflux of glucose from these cells. In conclusion, results suggest that zinc may play a pivotal role in the development of obesity concerning glucose metabolism.