Further studies with high-fat diet (HFD)-fed animal model of hyperlipidemia demonstrated that VK supplementation (5 μg/kg body weight, 8 weeks) reduced the plasma lipid levels, stimulated both the plasma levels and the hepatic protein expression of Gla-Gas6 protein, and regulated the AMPK/SREBP1/PPARα signaling pathways of hepatic lipid metabolism in HFD-fed mice.
Taken together, HDT inhibits OA-induced hepatic lipid accumulation via activation of AMPK and proliferator activated receptor-α/carnitine palmitoyltransferase signaling and enhancement of antioxidant activity as a potent candidate for nonalcoholic fatty liver disease and hyperlipidemia.
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.