Aronia melanocarpa Extract Ameliorates Hepatic Lipid Metabolism through PPARγ2 Downregulation

• Published in: PloS one Vol. 12; no. 1; p. e0169685
• Main Authors: Park, Chung-Hwa, Kim, Jung-Hee, Lee, Eun Byul, Hur, Wonhee, Kwon, Oh-Joo, Park, Hyoung-Jin, Yoon, Seung Kew
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 01.01.2017; Public Library of Science (PLoS)
• Subjects: Accumulation; Animals; Anthocyanins; Antioxidants; Aronia melanocarpa; Biochemical markers; Biology and Life Sciences; Body weight; Body Weight - drug effects; Cell Line; Diet, High-Fat; Down-Regulation - drug effects; Fatty acids; Fatty Acids, Nonesterified - pharmacology; Fatty liver; Fatty-acid synthase; Food; Gene expression; Genes; High fat diet; Hormones; Hyperlipidemia; Inhibition; Insulin resistance; Leptin; Leptin - analysis; Leptin - blood; Lipase; Lipid metabolism; Lipid Metabolism - drug effects; Lipids; Lipoprotein lipase; Lipoprotein Lipase - genetics; Lipoprotein Lipase - metabolism; Liver; Liver - drug effects; Liver - metabolism; Liver diseases; Male; Medicine and Health Sciences; Metabolic disorders; Metabolic syndrome; Metabolism; Mice; Mice, Inbred C57BL; Nutrition research; Photinia - chemistry; Photinia - metabolism; Plant Extracts - chemistry; Plant Extracts - pharmacology; PPAR gamma - antagonists & inhibitors; PPAR gamma - genetics; Protein biosynthesis; Protein synthesis; Research and Analysis Methods; RNA Interference; Rodents; Steatosis; Superoxide dismutase; Superoxide Dismutase - metabolism; Transaminases; Transaminases - blood; Triglycerides - analysis; Weight reduction; Western blotting
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0169685

Nonalcoholic fatty liver disease (NAFLD) is a hepatic manifestation of metabolic syndrome. Studies have demonstrated that anthocyanin-rich foods may improve hyperlipidemia and ameliorate hepatic steatosis. Here, effects of Aronia melanocarpa (AM), known to be rich of anthocyanins, on hepatic lipid metabolism and adipogenic genes were determined. AM was treated to C57BL/6N mice fed with high fat diet (HFD) or to FL83B cells treated with free fatty acid (FFA). Changes in levels of lipids, enzymes and hormones were observed, and expressions of adipogenic genes involved in hepatic lipid metabolism were detected by PCR, Western blotting and luciferase assay. In mice, AM significantly reduced the body and liver weight, lipid accumulation in the liver, and levels of biochemical markers such as fatty acid synthase, hepatic triglyceride and leptin. Serum transaminases, indicators for hepatocyte injury, were also suppressed, while superoxide dismutase activity and liver antioxidant capacity were significantly increased. In FL83B cells, AM significantly reduced FFA-induced lipid droplet accumulation. Protein synthesis of an adipogenic transcription factor, peroxisome proliferator-activated receptor γ2 (PPARγ2) was inhibited in vivo. Furthermore, transcriptional activity of PPARγ2 was down-regulated in vitro, and mRNA expression of PPARγ2 and its downstream target genes, adipocyte protein 2 and lipoprotein lipase were down-regulated by AM both in vitro and in vivo. These results show beneficial effects of AM against hepatic lipid accumulation through the inhibition of PPARγ2 expression along with improvements in body weight, liver functions, lipid profiles and antioxidant capacity suggesting the potential therapeutic efficacy of AM on NAFLD.