Ellagic acid attenuates high-carbohydrate, high-fat diet-induced metabolic syndrome in rats
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Fruits and nuts may prevent or reverse common human health conditions such as obesity, diabetes and hypertension; together, these conditions are referred to as metabolic syndrome, an increasing problem. This study has investigated the responses to ellagic acid, present in many fruits and nuts, in a diet-induced rat model of metabolic syndrome.
Eight- to nine-week-old male Wistar rats were divided into four groups for 16-week feeding with cornstarch diet (C), cornstarch diet supplemented with ellagic acid (CE), high-carbohydrate, high-fat diet (H) and high-carbohydrate, high-fat diet supplemented with ellagic acid (HE). CE and HE rats were given 0.8 g/kg ellagic acid in food from week 8 to 16 only. At the end of 16 weeks, cardiovascular, hepatic and metabolic parameters along with protein levels of Nrf2, NF-κB and CPT1 in the heart and the liver were characterised.
High-carbohydrate, high-fat diet-fed rats developed cardiovascular remodelling, impaired ventricular function, impaired glucose tolerance, non-alcoholic fatty liver disease with increased protein levels of NF-κB and decreased protein levels of Nrf2 and CPT1 in the heart and the liver. Ellagic acid attenuated these diet-induced symptoms of metabolic syndrome with normalisation of protein levels of Nrf2, NF-κB and CPT1.
Ellagic acid derived from nuts and fruits such as raspberries and pomegranates may provide a useful dietary supplement to decrease the characteristic changes in metabolism and in cardiac and hepatic structure and function induced by a high-carbohydrate, high-fat diet by suppressing oxidative stress and inflammation.
KeywordsCardiovascular remodelling Ellagic acid Metabolic syndrome Non-alcoholic fatty liver disease Obesity
This study was supported by Dr Red Nutraceuticals, Mt Nebo, QLD, Australia. This project was also partially funded by grants from The Prince Charles Hospital Foundation, Brisbane, QLD, Australia. We thank Mr. Paul Addison, School of Biomedical Sciences, and Mr. Brian Bynon, School of Veterinary Science, both at The University of Queensland, for their help with histopathological studies and plasma biochemical analyses, respectively. We also thank Dr. Thiruma V. Arumugam, School of Biomedical Sciences, The University of Queensland, for his assistance with Western blot analysis and Dr. Fiona Campbell, School of Veterinary Science, The University of Queensland, for her assistance with echocardiography.
Conflict of interest
No conflict of interest.
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