Vitisin A Regulates Lipid Metabolism in 3T3-L1 Adipocytes and High-Fat Diet-Induced Obese Mice

Obesity is a leading cause of various metabolic disorders, and its prevalence is rapidly increasing globally. In this study, we investigated the potential lipid-inhibitory and anti-obesity effects of oligostilbene compounds derived from Iris lactea in 3T3-L1 adipocytes. Particularly, Vitisin A on lipid accumulation in 3T3-L1 adipocytes, as well as on lipid metabolism in HFD-induced obese mice. The 3T3-L1 adipocytes and HFD-induced obese mice model were used in the study. In 3T3-L1 adipocytes, MTT assay, oil red O staining, transmission electron microscopy, MitoSox/DCFH-DA probe, and western blotting were used to assess specific indicators. In HFD-induced obese mice, lipid profile and hepatic injury were analyzed in the liver samples, histological sections were prepared and liver lipidomics analysis was performed, and western blotting was used to analyze the proteins associated with lipid lowering in Vitisin A. Vitisin A significantly reduced intracellular lipid accumulation, inhibited preadipocyte differentiation, and improved mitochondrial function in 3T3-L1 adipocytes. Transcriptomics analysis revealed notable changes in adipogenic gene expression in Vitisin A-treated 3T3-L1 cells. Furthermore, Vitisin A administration in HFD-induced obese mice resulted in smaller adipose depots and lower lipid concentrations. Lipidomics analysis indicated that Vitisin A modified lipid metabolic pattern in obese mice, significantly impacting triglycerols (TGs), phosphatidylcholines (PCs), and phosphatidylethanolamines (PEs). Mechanistic study revealed that Vitisin A is likely to activate the PPARγ/PGC-1α signaling pathway to ameliorating lipid metabolism disorders. The lipid-inhibitory and anti-obesity effects of Vitisin A from Iris lactea are regulated by lipid homeostasis and metabolism.