Regular physical activity is part of the public health recommendation for the prevention and the management of T2D and associated cardiovascular risks. Studies in mouse models showed that the subcutaneous adipose tissue could contribute to the beneficial effects of exercise training on glucose tolerance, partly by the secretion of exercise-induced adipokines. We aimed to identify novel exercise-induced factors in humans and study their effects on adipocyte and skeletal muscle. We characterized the leg adipose tissue transcriptomic response to an acute exercise bout in people with normal glucose tolerance (NGT) or type 2 diabetes (T2D), and sorted genes encoding for a potentially secreted protein that is significantly altered compared to the pre-exercise state (FDR>0,05). Results revealed 51 and 381 potentially secreted proteins significantly altered in both NGT and T2D adipose tissue in post-exercise and 3h-recovery state respectively. Among these genes, PLA2G2A, encoding for the secretory phospholipase A2 type IIA that has been associated with insulin sensitivity and metabolism, is distinctively upregulated in recovery state (logFC=0.9). In the present study, we aimed to understand the effect of PLA2G2A on adipocyte and skeletal muscle energy metabolism in vitro. The study includes PLA2G2A effects on gene expression profile, lipolysis, and fatty acid oxidation. We also checked the PLA2G2A levels in serum samples collected at the same time points. Our results suggests the autocrine/paracrine role of PLA2G2A on insulin sensitivity and lipid metabolism that may unravel its potential role in adipose tissue and skeletal muscle adaptation to exercise.