Barley sprout extract containing policosanols and polyphenols regulate AMPK, SREBP2 and ACAT2 activity and cholesterol and glucose metabolism in vitro and in vivo

• Administration of barley sprout extract (BS) improved plasma cholesterol, glucose, and hepatic lipid accumulation.
• BS suppressed cholesterol and glucose synthesis via AMPK activation.
• BS stimulated autophagy pathway via AMPK activation.
• BS could ameliorate hypercholesterolemia, hyperglycemia, and hepatic steatosis.

Mechanism of barley sprout extract (BS), which contains policosanols and polyphenols, on cholesterol and glucose metabolism was investigated. BS reduced the intracellular cholesterol concentrations in the HepG2 cells and the plasma cholesterol concentrations in the mice by the activation of AMPK and the subsequent phosphorylation inhibition of HMGCR. BS suppressed the nuclear translocation of SREBP2, reducing the transcription of HMGCR. AMPK activation with BS reduced the fasting glucose and hepatic triglyceride concentrations in mice by repressing the hepatic gluconeogenic genes, including fructose-1, 6-bisphosphatase and pyruvate carboxylase and the plasma levels of the proinflammatory cytokines tumor necrosis factor-α and interleukin-6. The activation of hepatic autophagy by BS was confirmed by induced protein expressions of LC3-II and LAMP. In conclusion, BS activates AMPK and hepatic autophagy and inhibits SREBP2, resulting in hypocholesterolemic and hypoglycemic activities and improvements in the symptoms of hepatic steatosis.