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Chlorogenic Acid Enriched in Coffee Pulp Extract Attenuates Hepatic Steatosis by Modulating Gene‐regulated Lipid Metabolism and Lipid Transporters
Author(s) -
Ontawong Atcharaporn,
Pasachan Tipthida,
Soodvilai Sunhapas,
Duangjai Acharaporn,
Pongchaidecha Anchalee,
Amornlerdpison Doungporn,
Srimareong Chutima
Publication year - 2018
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.2018.32.1_supplement.749.1
Subject(s) - lipogenesis , lipid metabolism , steatosis , cd36 , lipolysis , fatty acid synthase , chemistry , oil red o , fatty liver , pharmacology , biochemistry , lipid droplet , viability assay , biology , endocrinology , medicine , adipose tissue , cell , receptor , disease , adipogenesis
Background & Aims Coffee pulp (CP) is the first by‐product of coffee processing. Major constituents in CP include chlorogenic acid (CGA), epicatechin (EC), caffeine exhibited antioxidant, lipid lowering action, and several biological activities. However, it remains unknown whether CP rich CGA improved hepatic steatosis. This study aimed to investigate the effect of CP aqueous extract (CPE) on hepatic steatosis, and identified the mechanisms involved in hepatocellular carcinoma (HepG2) cells. Methods HepG2 cells at the cell density of 5×10 5 cells/well were pre‐incubated with CPE (10–200 μg/ml), CGA, and caffeine for 24 hr. Intracellular lipid accumulation was quantified using Nile red staining followed by flow cytometry. Cell viability of HepG2 cells was determined using MTT assay. The mRNA expression of genes involved in lipid metabolism and lipid transporters were also determined using quantitative real‐time PCR. Results CPE at the dose of 50–200 μg/ml, CGA, and caffeine significantly decreased lipid accumulation in HepG2 cells. Correspondingly, CPE decreased lipogenesis‐associated genes: PPARγ, and up‐regulated lipolysis‐related genes: PPARα. In addition, CPE reduced the lipid uptake transporter, FAT/CD36, while increased the lipid efflux transporters, ABCG5/8. Conclusion CPE has hepatic lipid‐lowering effects by modulating genes related lipolysis, lipogenesis, and lipid transporters. These findings indicate that anti‐hepatic steatosis by CPE is attributed to hepatic lipid‐lowering action for reversing such pathology. Thus, CPE could potentially be developed into nutraceutical product for prevention of non‐alcoholic fatty liver disease. Support or Funding Information This work was supported by the Faculty of Medicine Endowment Fund (066/2560 to CS), Chiang Mai University, the Research and Researcher for Industry (RRI) by Thailand Research Fund (TRF) (PHDI0010 to CS), and the NSTDA Chair Professor grant (the Fourth Grant) of the Crown Property Bureau Foundation and the National Science and Technology Development Agency to Professor Dr. Vatcharin Rukachaisirikul. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .