Cocoa protective effects against abnormal fat storage and oxidative stress induced by a high-fat diet involve PPARα signalling activation

Food Funct. 2014 Nov;5(11):2931-9. doi: 10.1039/c4fo00616j.


A high-fat (HF) diet increases lipid storage and oxidative stress in mouse liver and this process seems to be mediated by Peroxisome Proliferator-Activated Receptor α (PPARα). In this study we evaluated the protective effect of cocoa against hepatic steatosis induced by a HF diet. The HF diet down-regulated PPARα expression and turned off PPARα-signalling, deregulated the β-oxidation (β-Ox) system and catalase (CAT) activity, increased fat storage, reduced expression of enzymatic activity involved in oxidative defence in the liver and doubled the weight gain per calorie consumed compared to animals under the normal diet. In contrast, cocoa improved hepatic β-Ox, activated PPARα-signalling and up-regulated both gene and protein expression of SOD1. Moreover, when co-administered with the HF diet, cocoa treatment counteracted lipid storage in the liver, improved the lipid-metabolizing activity and oxidative stress defences and normalized the weight gain per calorie consumed.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Abdominal Fat / drug effects*
  • Abdominal Fat / metabolism
  • Animals
  • Body Weight
  • Cacao / chemistry*
  • Diet, High-Fat / adverse effects
  • Energy Intake
  • Fatty Liver / etiology
  • Fatty Liver / prevention & control
  • Liver / drug effects
  • Liver / metabolism
  • Male
  • Mice
  • Oxidative Stress / drug effects*
  • PPAR alpha / genetics
  • PPAR alpha / metabolism*
  • Phytotherapy / methods*
  • Plant Preparations
  • Signal Transduction


  • PPAR alpha
  • Plant Preparations