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Barley sprout extract containing policosanols and polyphenols regulate AMPK,SREBP2 and ACAT2 activity and cholesterol and glucose metabolism in vitro and in vivo
Affiliation:1. Department of Food Bioscience and Technology, College of Life Sciences and Biotechnology, Korea University, Seoul, 136-713, Republic of Korea;2. Department of Biotechnology, Graduate School of Life Sciences and Biotechnology, Korea University, BK21-PLUS, Seoul, 136-713, Republic of Korea;3. Department of Functional Crop, National Institute of Crop Science (NICS), Rural Development Administration (RDA), Miryang, 627-803, Republic of Korea;1. Department of Pharmacology, Pharmacotherapy and Toxicology Faculty of Pharmacy, Medical University of Sofia, 2 Dunav St., 1000 Sofia, Bulgaria;2. Department of Pharmacognosy, Faculty of Pharmacy, Medical University of Sofia, 2 Dunav St., 1000 Sofia, Bulgaria;1. State Key Laboratory of Food Science and Technology, Nanchang University, Nanchang 330047, PR China;2. Guelph Food Research Centre, Agriculture and Agri-Food Canada, 93 Stone Road West, Guelph, Ontario NIG 5C9, Canada;3. Glyn O. Phillips Hydrocolloid Research Centre, Glyndŵr University, Wrexham LL11 2AW, UK;4. Phillips Hydrocolloids Research Ltd., 45 Old Bond Street, London W1S 4QT, UK
Abstract: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.
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