Obesity is a low-grade sustained inflammatory state that causes oxidative stress 
in different metabolic tissues, which leads to insulin resistance and 
nonalcoholic fatty liver disease (NAFLD). Particularly, obesity-induced 
metabolic endotoxemia plays an important role in the pathogenesis of insulin 
resistance and inflammation. Nuclear factor erythroid 2-related factor 2 (Nrf2) 
is a key regulator of antioxidant signaling that serves as a primary cellular 
defense against the cytotoxic effects of oxidative stress. Pharmacological 
stimulation of Nrf2 mitigates obesity and insulin resistance in mice; however, 
Nrf2 activators are not clinically available due to biosafety concerns. A recent 
study demonstrated that glucoraphanin, a precursor of the Nrf2 activator 
sulforaphane, ameliorates obesity by enhancing energy expenditure and browning 
of white adipose tissue, and attenuates obesity-related inflammation and insulin 
resistance by polarizing M2 macrophages and reducing metabolic endotoxemia. 
Thus, this review focuses on the efficiency and safety of glucoraphanin in 
alleviating obesity, insulin resistance, and NAFLD. Abbreviations: ALT, Alanine 
aminotransferase; AMPK, AMP-activated protein kinase; ATMs, Adipose tissue 
macrophages; BAT, Brown adipose tissue; CDDO-Im, 
2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid-imidazolide; CDDO-Me, CDDO-methyl 
ester; DIO, High-fat-diet-induced obese; FFA, Free fatty acid; FGF, Fibroblast 
growth factor; GTP, Glutamyl transpeptidase; HFD, High-fat diet; IKKβ, Inhibitor 
of κB-kinase β; IL, Interleukin; JNK, C-Jun N-terminal kinase; KD, Knockdown; 
Keap1, Kelch-like ECH-associated protein 1; KO, Knockout; LPS, 
Lipopolysaccharide; NADPH, Nicotinamide adenine dinucleotide phosphate; NAFLD, 
Non-alcoholic fatty liver disease; NF-κB, Nuclear factor-κB; Nrf2, Nuclear 
factor E2-related factor 2; ROS, Reactive oxygen species; T2D, Type 2 diabetes; 
TLR, Toll-like receptor; TNF, tumor necrosis factor; UCP, Uncoupling protein; 
WAT, White adipose tissue.