Latanoprost functioned as both an indirect activator of AMP-activated protein kinase and a selective retinoid X receptor α (RXRα) antagonist able to selectively antagonise the transcription of a RXRα/peroxisome proliferator-activated receptor γ heterodimer. Latanoprost induced morphological abnormality and viability decline of HCS cells in vitro. It induces cell cycle arrest of HCS cells. Latanoprost induces abnormal changes of plasma membrane, DNA fragmentation and ultrastructural abnormality of HCS cells. Caspase activation in HCS cells is also activated by Latanoprost treatment. Latanoprost induces MTP disruption and quantitative changes of mitochondrion-associated pro-apoptotic regulators in HCS cells. Latanoprost is effective in inhibiting adipogenesis, reducing lipogenesis, promoting fatty acid oxidation and enhancing GLUT4 translocation and glucose uptake both in adipocytes and myotubes.