We used for that a model of equine ASCs in which PPARγ has been silenced using siRNA transfection, and investigated the outcomes of SHBG treatment in terms of cell viability, apoptosis, premature senescence and mitochondrial functions to determine whether SHBG may represent a potential PPARγ mimic for future clinical application in the management of metabolic disorders. The gene discussed is SHBG; the disease is metabolic disease.