## 4 Discussion
Unexpectedly, the promoted glucose intake in our study could be explained by the stimulated insulin signaling pathway only in P4, where we found upregulation in mRNA gene expression of PI3K and Slc2a4, coding the GLUT4 protein. The lack of alteration in the lipolysis rate and intracellular lipid deposition in this group, alongside an increased glucose flux by 41%, suggests stimulated beta-oxidation. Increased beta-oxidation after-probiotic administration in mice and 3T3-L1 cells was reported by [PERSON] et al. [16], further manifested by a proven weight loss effect. In the rest of the _L. paracasei_ CFS-treated groups, the Slc2a4 gene expression was similar (in M2.1) or downregulated (in C8 and C15) compared to the control (MRS_C). At the same time, the increased glucose consumption remained approximately the same compared to P4. These supernatants significantly upregulate the Slc2a1-GLUT1 protein-coding gene expression, which is responsible for basal glucose uptake in many cell types, including adipocytes. Like GLUT4, the final step of GLUT1's physiological role realization is its translocation to the cell surface. Several extracellular stimuli are shown to modulate this process, but kinetic analyses indicate that the insulin impact is negligible. Thus, its expression levels remain almost unchanged in a diabetic state [53; 54]. It should be emphasized that in adipose tissue, GLUT1-mediated glucose transport is less effective than GLUT4 ones [54], and the increased activity of GLUT1 is more likely to contribute to adipocyte glucose uptake only in preserved GLUT4 functionality. Therefore, the facilitated glucose influx in group M2.1 was most likely due to the upregulation of Slc2a1 mRNA gene expression, where no suppression of Slc2a4, PI3K, or IRS-1 expression was observed. The increased glucose uptake via an insulin-independent pathway without suppressing insulin signaling that was observed in this group could benefit existing insulin resistance or type II diabetes. Additionally, we established an increased neutral lipid deposition and a significant decrease in lipolysis rate or the so-called \"healthy expansion\" of adipocytes, which is extremely valuable in the presence of factors highly predisposing to obesity. The obtained results from the C8 and C15 groups appear controversial. In fact, the data indicated an effect similar to that of M2.1. Moreover, the suppressed lipolysis and intensified glucose uptake were not accompanied by increased intracellular lipid deposition, which indicates a potentiated beta-oxidation. The gene analyses in these groups noted a decreased mRNA expression of PPARy--a highly desired effect of food additives preventing obesity. However, considering that mature adipocytes were used in our study, the gene expression analyses in C8 and C15 outlined likely adverse health outcomes. Plenty of evidence indicates the pivotal role of PPARy in metabolic homeostasis in adipose tissue physiology. It has been widely adopted as a classical drug target for ameliorating metabolic syndrome and type 2 diabetes. PPARy triggers a subtle network of transcriptional changes in early adipogenic differentiation. So far, no transcriptional factor has been found to promote preadipocyte adipogenic differentiation in the absence of PPARy [55]. PPARy also remains essential for maintaining homeostasis in mature adipocytes. Its ablation from adult mouse adipocytes makes them prone to apoptosis [56]. Recently, it has been clarified that in lean mice models, the PPARy1 isoform plays a central role in adipose tissue development and function. In a high-fat state, PPARy2 is crucial for balancing energy expenditure and intracellular lipid deposition, being a critical factor in adipose total storage capacity and healthy expandability [55; 57]. Its inhibited expression is concomitant with detrimental adipocyte hypertrophy, mitochondrial dysfunction, and adipose tissue inflammation, which are strongly associated with obesity-associated metabolic complications, including insulin-deficient diabetes [58; 59].