Non-drug strategy targeting adipocyte differentiation is critical for alleviating visceral obesity and its related diseases. However, whether and how low intensity pulsed ultrasound (LIPUS) could be used for inhibiting visceral adipocyte differentiation is not fully understood. In this study, we aim to investigate the effect and associated mechanism of LIPUS on primary visceral preadipocyte differentiation and explore its potential role for clinical visceral obesity management. The preadipocytes were daily exposed to LIPUS (0.5 MHz, 1.2 MPa) for 10 min. Adipogenic differentiation was estimated by the formation of lipid droplets and the levels of adipogenic transcriptional factors and representative markers. Mitogen-activated protein kinase (MAPK) member proteins and histone acetylation-related molecules were measured by western blotting. LIPUS stimulation with an average acoustic pressure of 1.2 MPa led to a prominent inhibition of adipogenic differentiation and expression of adipogenic markers. As a mechanism, LIPUS treatment increased the nuclear levels of histone deacetylase 1 (HDAC1) and decreased the acetylation of histone 3 and histone 4. Meanwhile, the inhibition of the HDAC1 could block the inhibitory effect of LIPUS on adipogenic differentiation via increasing AcH3 and AcH4 levels. Our study may provide an ultrasound-based promising strategy for clinical visceral obesity control.
Keywords: C/EBPs; HDAC1; LIPUS; PPARγ; adipogenic differentiation; preadipocyte.