These findings suggest that DPP4 functions as an important mediator of chronic stress‐stimulated adipose inflammation and dysfunction via the modulation of adipocyte oxidative stress production and apoptosis that is mediated by the GLP‐1/PI3K‐AKT axis, indicating that DPP4 inhibition and/or GLP‐1R stimulation may have applications for treating metabolic disorders of patients under chronic stress conditions. The gene discussed is AKT1; the disease is metabolic disease.