Sulforaphane Improves Lipid Metabolism by Enhancing Mitochondrial Function and Biogenesis In Vivo and In Vitro

Scope Sulforaphane (SFN) is reported to reduce the accumulation of lipids. However, the underling mechanism remains unclear. In this study, the potential of SFN to improve lipid metabolism is investigated through altering mitochondrial function and biogenesis-related mechanisms. Methods and Results The abnormal lipid metabolism model was established both in HHL-5 cells and in rats by feeding a high-fat diet (HFD) for 10 weeks. The current findings suggest that SFN alleviates the swelling of mitochondria and stimulates mitochondrial biogenesis. The reduced expression of NRF1 and TFAM, were reversed by SFN. SFN increases the levels of antioxidant compounds via nuclear factor erythroid-2-related factor (Nrf2) activation. Furthermore, SFN improves multiple mitochondrial bioactivities, such as mitochondrial membrane potential, ATP, and the electron transfer chain based on PGC-1 alpha pathway. SFN also activates lipolysis by transcriptionally upregulating adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL). Conclusions SFN enhances utilization of lipids via both the PGC- 1 alpha-dependent promotion of mitochondrial biogenesis and Nrf2 dependent improvement of mitochondrial function.