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Rosemary extract regulates glucose and lipid metabolism by activating AMPK and PPAR pathways in HepG2 cells
Author(s) -
Tu Zheng Alex,
MossPierce Tijuana,
Ford Paul,
Jiang Alan
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.247.5
Subject(s) - ampk , endocrinology , amp activated protein kinase , lipid metabolism , medicine , carbohydrate metabolism , beta oxidation , peroxisome proliferator activated receptor , glycolysis , gluconeogenesis , metabolic pathway , chemistry , glucose uptake , fatty acid metabolism , protein kinase a , biology , metabolism , biochemistry , kinase , receptor , insulin
An epidemic of metabolic disorders such as diabetes and obesity is rising dramatically, affecting ~30% of the US adult population. Using natural products as potential therapeutic and preventive interventions has drawn worldwide attention. Rosemary has been shown to lower blood glucose, cholesterol levels and mitigate weight gain in several in vivo studies; however, the mechanisms are essentially unknown. We investigated the effects of rosemary on metabolism in hepatocyte HepG2 and demonstrated that rosemary extracts (RE) significantly increase glucose consumption by 21%. The phosphorylation of AMP‐activated protein kinase (AMPK), as well as its substrate, acetyl‐CoA carboxylase (ACC) was increased by RE treatment. RE also transcriptionally regulate genes involved in metabolism, including SIRT1 (up 2.9‐fold), PPARγ coactivator 1α (PGC1α, up 1.7‐fold), low density lipoprotein receptor (up 2‐fold), glucose‐6‐phosphatase (down 65%), and ACC (down 32%). Furthermore, the PPARγ specific antagonist GW9662 diminished rosemary's effects on glucose consumption, indicating PPAR pathways contribute to rosemary's effects. Overall, our study suggested that RE potentially increase liver glycolysis and fatty acid oxidation, while decrease gluconeogenesis and fatty acid synthesis by activating the AMPK and PPAR pathways.