Fucoidan is a polysaccharide largely made up of l-fucose and sulfate groups. Fucoidan is favorable worldwide, especially amongst the food and pharmaceutical industry as a consequence of its promising therapeutic effects. Its applaudable biological functions are ascribed to its unique biological structure. Classical bioactivities associated with fucoidan include anti-oxidant, anti-tumor, anti-coagulant, anti-thrombotic, immunoregulatory, anti-viral and anti-inflammatory effects. More recently, a variety of in vitro and in vivo studies have been carried out to further highlight its therapeutic potentials. This review focuses on the progress towards understanding fucoidan and its biological activities, which may be beneficial as a future therapy. Hence, we have summarized in vitro and in vivo studies that were done within the current decade. We expect this review and a variety of others can contribute as a theoretical basis for understanding and inspire further product development of fucoidan.

Insulin resistance is a characteristic feature of type 2 diabetes. Sulforaphane (SFN) is a natural antioxidant extracted from the cruciferous vegetables. Recent study reported that SFN exhibits excellent anti-diabetic effects, however, the underlying mechanism is still unclear. This study aimed to investigate the therapeutic effects of SFN on a high-fat diet (HFD)-induced insulin resistance and potential mechanism. SFN was found to effectively reduce body weight, fasting blood glucose and hyperlipidemia, and improve liver function in HFD-fed mice. Furthermore, SFN effectively increased glucose uptake and improved insulin signaling in palmitic acid (PA)-induced HepG2 cells. SFN also led to increased expression of antioxidant genes downstream of Nrf2 and decreased accumulation of lipid peroxides MDA and 4-HNE, both in vivo and in vitro. Further studies revealed that SFN significantly reduced glutathione peroxidase 4 (GPx4) inactivation-mediated oxidative stress by activating the AMPK and Nrf2 signaling pathways. In PA-induced HepG2 cells and flies, the alleviation of insulin resistance by SFN was diminished by GPx4 inhibitor. Taken together, SFN ameliorated HFD-induced insulin resistance by activating the AMPK-Nrf2-GPx4 pathway, providing new insights into SFN as a therapeutic compound for the alleviation of insulin resistance.