White adipose tissue is the largest endocrine organ in the body, which through endocrine or paracrine mechanisms, communicates with several tissues. Our preliminary study involved two independent experiments. The primary objective of Experiment 1 was to examine the effect of co-incubating Caco-2- derived enterocytes with human preadipocytes (HPAd)-derived adipocytes on cellular processes in the studied cells. Experiment 2 aimed to explore the impact of co-incubation of adipocytes with Caco-2-derived enterocytes on bacterial adhesion of conventional and pathogenic bacterial strains to Caco-2 cells and their viability after treatment with the studied bacteria. Caco-2 cells were seeded in inserts, and on the day of the experiment, these inserts with fully differentiated enterocytes were transferred to plates containing fully differentiated adipocytes. This approach created a model where metabolites from adipocytes contacted enterocytes from the opposite side of the intestinal lumen, simulating the conditions found in obese individuals, where visceral fat covers internal organs, including the intestines. Furthermore, due to the observed persistent inflammation in obese individuals resulting from the excess visceral fat, some groups of HPAd cells were stimulated with lipopolysaccharide (LPS) to induce the synthesis of inflammatory agents. Based on the data obtained in in vitro experiments, it can be concluded that the co-incubation of Caco-2 cells with adipocytes positively affects cellular processes occurring in Caco-2 cells by reducing the expression of proinflammatory cytokines and apoptosis markers. Moreover, pre-incubation of Caco-2 enterocytes with adipocytes protects these cells against Salmonella enterica by reducing bacterial adhesion and increasing the viability of Caco-2 cells. Incubation of Caco-2-derived enterocytes with LPS-pre-treated adipocytes did not cause significant changes compared to non-treated adipocytes.