The changes in PPARγ2 protein expression were assessed in mice livers.

<p>Western blot analysis showed increase of PPARγ2 protein expression in HFD group and suppression of the protein in HFD+AM group (A) although the suppression was not statistically significant (B).</p

<i>Aronia melanocarpa</i> Extract Ameliorates Hepatic Lipid Metabolism through PPARγ2 Downregulation

<div><p>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 <i>Aronia melanocarpa</i> (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 <i>in vivo</i>. Furthermore, transcriptional activity of PPARγ2 was down-regulated <i>in vitro</i>, and mRNA expression of PPARγ2 and its downstream target genes, adipocyte protein 2 and lipoprotein lipase were down-regulated by AM both <i>in vitro</i> and <i>in vivo</i>. 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.</p></div

mRNA expressions of transcription factors related with hepatic lipid metabolsim were assessed.

<p>Changes of PPARγ2, SREBP1c, ChREBP and PPARα expressions from mice livers were analyzed by RT-PCR (A), and AM significantly inhibited HFD-induced PPARγ2 expression (B).</p

AM improves HFD-induced redox imbalance.

<p>Hepatic SOD activity (A) and TEAC (B) were decreased in HFD group, but these were significantly increased in HFD+AM group.</p

AM affects HFD-induced lipogenesis, hepatocellular injury and leptin level.

<p>While HFD induced significant elevation in intrahepatic TG (A), FAS (B), serum ALT (C), AST (D) and leptin (E), these were significantly inhibited in HFD+AM group.</p

AM prevents HFD-induced intrahepatic lipid accumulation and weight gain.

<p>Hepatic steatosis was reduced in HFD+AM group both grossly (A) and histologically (B; H&E stain, magnification 100×). HFD-induced increase of body and liver weight were also significantly deterred by AM (C).</p

Nile-red stain was performed to show lipid droplets in FFA treated cells.

<p>FFA-induced lipid droplets were reduced in AM treated cells (bright red spots, A), and fluorometry revealed that AM reduced lipid droplets dose-dependently while FFA treatment increased lipid droplets over twofold of the control.</p

Primer sequences used for RT-PCR.

<p>Primer sequences used for RT-PCR.</p