Dietary açai attenuates hepatic steatosis via adiponectin-mediated effects on lipid metabolism in high-fat diet mice Joyce Ferreira da Costa Guerra a , Poliane Silva Maciel b , Isabel Cristina Mallosto Emerich de Abreu b , Renata Rebeca Pereira a,c , Maisa Silva d , Leandro de Morais Cardoso e , Helena Maria Pinheiro-Sant’Ana f , Wanderson Geraldo de Lima c , Marcelo Estáquio Silva g , Maria Lúcia Pedrosa a,c, * a Biological Research Center, Federal University of Ouro Preto, Ouro Preto, MG, Brazil b School of Nutrition, Federal University of Ouro Preto, Ouro Preto, MG, Brazil c Department of Biological Sciences, Federal University of Ouro Preto, Ouro Preto, MG, Brazil d Department of Basic Health, Federal University of Juiz de Fora, Governador Valadares Campus, Governador Valadares, MG, Brazil e Department of Nutrition, Federal University of Juiz de Fora, Governador Valadares Campus, Governador Valadares, MG, Brazil f Department of Nutrition and Health, Federal University of Viçosa, Viçosa, MG, Brazil g Department of Food Science, Federal University of Ouro Preto, Ouro Preto, MG, Brazil ARTICLE INFO Article history: Received 9 December 2014 Received in revised form 16 January 2015 Accepted 20 January 2015 Available online 13 February 2015 ABSTRACT Polyphenols, especially anthocyanins, have been considered promising for the prevention of nonalcoholic fatty liver disease (NAFLD). This study investigated whether açai (Euterpe oleracea Mart.), a source of anthocyanins and recognized as one of the new “superfruits”, could alleviate high-fat diet (HFD)-induced NAFLD in mice. In HFD mice, aqueous açai extract (AAE) administration (3 g/kg) for six weeks improved insulin resistance index and in- creased adiponectin mRNA expression in adipose tissue and serum levels. Furthermore, AAE decreased the total liver triacylglycerol content and attenuated HFD-induced hepatic ste- atosis. This reduced hepatic lipid content was associated with AAE-mediated up-regulation of genes involved in adiponectin signaling, including adiponectin receptor 2, PPAR-α, and its target gene, carnitine palmitoyltransferase.Thus, dietary açai can protect liver from ste- atosis through its enhancement of adiponectin levels, improvement of insulin sensitivity, and increase in PPAR-α-mediated fatty acid oxidation. © 2015 Elsevier Ltd. All rights reserved. Keywords: Euterpe oleracea mart Anthocyanins Nonalcoholic fatty liver disease Insulin resistance Adipokines Peroxisome proliferator-activated receptor α * Corresponding author. Biological Research Center, Federal University of Ouro Preto, Ouro Preto, MG, Brazil.Tel.: +55 3135591696; fax: +55 3135591696. E-mail address: lpedrosa@nupeb.ufop.br (M.L. Pedrosa). Abbreviations: ACC, acetyl coenzyme A carboxylase; AdipoR2, adiponectin receptor 2; ALT, alanine aminotransferase; AST, aspartate aminotransferase; CPT-1, carnitine palmitoyltransferase 1; C3G, cyanidin 3-glucoside; DPPH, 2,2-diphenyl-1-picrylhydrazil; FAS, fatty acid synthase; FAT, fatty acid translocase; FFA, free fatty acid; HOMA-IR, homeostasis model assessment of insulin resistance; IL-6, interleukin 6; IR, insulin resistance; NAFLD, nonalcoholic fatty liver disease; PPAR, peroxisome proliferator-activated receptor; SREBP-1c, sterol regu- latory element-binding protein-1c; TG, triacylglycerol; TNFα, tumor necrosis factor α; Trolox, 6-hydroxy-2,5,7,8-tetramethylchroman-2- carboxylic acid; UCP-2, uncoupling protein 2; WAT, white adipose tissue Chemical compounds: Cyanidin 3-rutinoside (PubChem CID: 29231); Cyanidin 3-glucoside (PubChem CID: 197081). http://dx.doi.org/10.1016/j.jff.2015.01.025 1756-4646/© 2015 Elsevier Ltd. All rights reserved. journal of functional foods 14 (2015) 192–202 Available online at www.sciencedirect.com ScienceDirect journal homepage: www.elsevier.com/locate/jff