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The aim of this study was to investigate the anti-obesity and antihyperlipidemic efficacy and molecular mechanisms of Aster spathulifolius Maxim extract (ASE) in rats with high-fat diet (HFD)-induced obesity. Rats were separately fed a normal diet or a HFD for 8 weeks, then they were treated with ASE (62.5, 125, or 250 mg/kg) for another 4.5 weeks. The ASE supplementation significantly lowered body weight gain, visceral fat pad weights, serum lipid levels, as well as hepatic lipid levels in HFD-induced obese rats. Histological analysis showed that the ASE-treated group showed lowered numbers of lipid droplets and smaller size of adipocytes compared to the HFD group. To understand the mechanism of action of ASE, the expression of genes and proteins involved in obesity were measured in liver and skeletal muscle. The expression of fatty acid oxidation and thermogenesis-related genes (e.g., PPAR-α, ACO, CPT1, UCP2, and UCP3) of HFD-induced obese rats were increased by ASE treatment. On the other hand, ASE treatment resulted in decreased expression of fat intake-related gene ACC2 and lipogenesis-related genes (e.g., SREBP-1c, ACC1, FAS, SCD1, GPATR, AGPAT, and DGAT). Furthermore, ASE treatment increased the level of phosphorylated AMPKα in obese rats. Similarly, the level of phosphorylated ACC, a target protein of AMPKα in ASE groups, was increased by ASE treatment compared with the HFD group. These results suggest that ASE attenuated visceral fat accumulation and improved hyperlipidemia in HFD-induced obese rats by increasing lipid metabolism through the regulation of AMPK activity and the expression of genes and proteins involved in lipolysis and lipogenesis.

ObjectivesA ster spathulifolius Maxim (AS), known for its anti-viral and anti-allergic activity, is also known to reduce body weight gain in high fat diet-induced obese rats. But its molecular mechanism of the anti-obesity effects is still unclear. So, we investigated the inhibitory effect of AS extract (ASE) on adipogenesis and lipid accumulation to determine the underlying cellular molecular mechanism.MethodsTo perform this study, the contents of intracellular triglyceride were analysed. Real-time polymerase chain reaction and Western blotting were carried out to investigate the expression of adipogenic transcriptional factors.Key findingsASE showed the suppression of adipogenic differentiation and the considerable reduction of the lipid accumulation in 3T3-L1 cells. Especially, ASE inhibited the early stage of differentiation via the downregulation of C/EBP-β and C/EBP-δ, which are early adipogenic factors. Major adipogenic factors, such as PPAR-γ and C/EBP-α, were also subsequently inhibited. These findings were supported by Oil Red O staining and intracellular triglyceride levels. A molecular mechanism liking the effect of ASE was identified through the activation of AMPKα pathway. ASE increased protein levels of phosphorylated AMPKα and phosphorylated ACC.ConclusionsASE showed anti-adipogenic and anti-lipogenic effects through the regulation of adipogenic factors and AMPKα pathway.