High-fat-diet (HFD) feeding is associated with liver oxidative stress (OS), n-3 long-chain polyunsaturated fatty acid (n-3 LCPUFA) depletion, hepatic steatosis and mitochondrial dysfunction. Our hypothesis is that the HFD-induced liver injury can be attenuated by the combined supplementation of n-3 LCPUFA eicosapentaenoic acid (EPA) and the antioxidant hydroxytyrosol (HT). The C57BL/6J mice were administered an HFD (60% fat, 20% protein, 20% carbohydrates) or control diet (CD; 10% fat, 20% protein, 70% carbohydrates), with or without EPA (50 mg kg⁻¹ day⁻¹), HT (5 mg kg⁻¹ day⁻¹), or EPA + HT (50 and 5 mg kg⁻¹ day⁻¹, respectively) for 12 weeks. We measured the body and liver weights and dietary and energy intakes along with liver histology, FA composition, steatosis score and associated transcription factors, mitochondrial functions and metabolic factors related to energy sensing through the AMP-activated protein kinase (AMPK) and PPAR-γ coactivator-1α (PGC-1α) cascade. It was found that the HFD significantly induced liver steatosis, with a 66% depletion of n-3 LCPUFAs and a 100% increase in n-6/n-3 LCPUFA ratio as compared to the case of CD (p < 0.05). These changes were concomitant with (i) a 95% higher lipogenic and 70% lower FA oxidation signaling, (ii) a 40% diminution in mitochondrial respiratory capacity and (iii) a 56% lower ATP content. HFD-induced liver steatosis was also associated with (iv) a depressed mRNA expression of AMPK-PGC-1α signaling components, nuclear respiratory factor-2 (NRF-2) and β-ATP synthase. These HFD effects were significantly attenuated by the combined EPA + HT supplementation in an additive manner. These results suggested that EPA and HT co-administration partly prevented HFD-induced liver steatosis, thus strengthening the importance of combined interventions in hepatoprotection in non-alcoholic fatty liver disease.

During frying, oils can deteriorate due to autoxidation and hydrolytic alterations, processes influenced by the oil's fatty acid composition (FAC) and antioxidant content. However, there are different techniques to improve fried food quality and reduce oil absorption. This review aims to assess existing literature on the interactions between frying methods, oil selection, and the chemical composition of foods. To achieve this goal, the article examines the impact of oil FAC, antioxidants, pretreatments, and alternative frying technologies. A literature search was conducted from 2016 to 2023. The keywords used were (AND/OR) frying, fried foods, oil, oil absorption, and fatty acids. Oils rich in monounsaturated fatty acids and antioxidants, such as olive oil, are recommended for their nutritional benefits and improved oil stability. The water content and structure of the food also play a significant role in oil absorption. Pretreatments to diminish food moisture content contribute to a lower oil absorption in the fried food while mitigating excessive accumulation of lipid oxidation products. Proper selection of frying oils, incorporation of antioxidants, and the use of pretreatments could help prevent chemical changes and minimize oil absorption during frying. These measures contribute to maintaining the nutritional quality and safety of fried foods while also enhancing their overall sensory appeal.

Pharmacological therapy for nonalcoholic fatty liver disease (NAFLD) is not approved at the present time. For this purpose, the effect of combined eicosapentaenoic acid (EPA; 50 mg/kg/day) modulating hepatic lipid metabolism and hydroxytyrosol (HT; 5 mg/kg/day) exerting antioxidant actions was evaluated on hepatic steatosis and oxidative stress induced by a high‐fat diet (HFD; 60% fat, 20% protein, and 20% carbohydrates) compared to a control diet (CD; 10% fat, 20% protein, and 70% carbohydrates) in mice fed for 12 weeks. HFD‐induced liver steatosis (i) was reduced by 32% by EPA, without changes in oxidative stress‐related parameters and mild recovery of Nrf2 functioning affording antioxidation and (ii) was decreased by 42% by HT, concomitantly with total regain of the glutathione status diminished by HFD, 42% to 59% recovery of lipid peroxidation and protein oxidation enhanced by HFD, and regain of Nrf2 functioning, whereas (iii) combined EPA + HT supplementation elicited 74% reduction in liver steatosis, with total recovery of the antioxidant potential in a similar manner than HT. It is concluded that combined HT + EPA drastically decreases NAFLD development, an effect that shows additivity in HT and EPA effects that mainly relies on HT, strengthening the impact of oxidative stress as a central mechanism underlying liver steatosis in obesity.