GPT and Hepatic fibrosis: Decreased lipids in 3T3-L1 adipocytes by downregulating adipogenic transcription factors, sterol regulatory element-binding protein 1c, CCAAT/enhancer-binding protein α, peroxisome proliferator-activated receptor γ, and lipid accumulation-related genes adipocyte protein-2, as well as fatty acid synthase. Decreased ALT, AST, TG levels. Deceased expression of iNO synthase, suppression of the inactivation of macrophages, and Kupffer cells in liver. Inhibition of α-smooth muscle actin, transforming growth factor β-1, and collagen type-I α-1 chain leading to reduced liver fibrosis.