Abstract

Long-term high-fat diet (HFD) consumption can cause weight gain and obesity, two conditions often associated with hepatic non-alcoholic fatty liver and oxidative stress. Oleoylethanolamide (OEA), a lipid compound produced by the intestine from oleic acid, has been associated with different beneficial effects in diet-induced obesity and hepatic steatosis. However, the role of OEA on hepatic oxidative stress has not been fully elucidated. In this study, we used a model of diet-induced obesity to study the possible antioxidant effect of OEA in the liver. In this model rats with free access to an HFD for 77 days developed obesity, steatosis, and hepatic oxidative stress, as compared to rats consuming a low-fat diet for the same period. Several parameters associated with oxidative stress were then measured after two weeks of OEA administration to diet-induced obese rats. We showed that OEA reduced, compared to HFD-fed rats, obesity, steatosis, and the plasma level of triacylglycerols and transaminases. Moreover, OEA decreased the amount of malondialdehyde and carbonylated proteins and restored the activity of antioxidant enzymes superoxide dismutase, catalase, and glutathione peroxidase, which decreased in the liver of HFD-fed rats. OEA had also an improving effect on parameters linked to endoplasmic reticulum stress, thus demonstrating a role in the homeostatic control of protein folding. Finally, we reported that OEA differently regulated the expression of two transcription factors involved in the control of lipid metabolism and antioxidant genes, namely nuclear factor erythroid-derived 2-related factor 1 (Nrf1) and Nrf2, thus suggesting, for the first time, new targets of the protective effect of OEA in the liver.

Highlights

  • It is widely accepted that lifestyle plays a fundamental role in maintaining a healthy status

  • We reported that a two-week treatment with OEA to rats exposed to an high-fat diet (HFD) exerts anti-obesity effects and ameliorates both liver steatosis and hepatic stress, two conditions associated with diet-induced obesity

  • We highlighted a critical role for both nuclear factor erythroid-derived 2-related factor 1 (Nrf1) and nuclear factor erythroid-derived 2-related factor 2 (Nrf2) in OEA-induced antioxidant and antisteatotic effects

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Summary

Introduction

It is widely accepted that lifestyle plays a fundamental role in maintaining a healthy status. Increased intake of high-palatable energy-dense foods, rich in sugars and lipids, predisposes the organism in the long-term to numerous metabolic diseases. Obesity is characterized by an increase in body fat, caused by an energy imbalance, especially when consuming fat-rich diets. High-fat consumption, typical of the so-called Western diets, has been associated with insulin resistance, dyslipidemia, and metabolic/cardio-. High-fat diet (HFD)-associated obesity is very common in patients affected by non-alcoholic fatty liver disease (NAFLD), which represents one of the most frequent causes of liver disease, in Western countries [1,2,3]. NAFLD is characterized by excessive hepatic lipid accumulation [4] and is recognized as the typical hepatic manifestation of metabolic syndrome [5]. Several lines of evidence suggest that a plethora of dysfunctional processes occur during the progression of NAFLD including inflammation, mitochondrial and endoplasmic reticulum (ER) impairment and oxidative stress [6,7,8,9]

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