Abstract
The present study aimed to investigate the intervention of selenium in the oxidative stress and apoptosis of pig livers, which were induced by a high-fat diet, and the effects of four endoplasmic reticulum (ER)-resident selenoproteins in the process. A 2 × 4 design trial was conducted that included two dietary fat levels (BD = basal diet and HFD = high-fat diet) and four dietary Se supplementation levels (0, 0.3, 1.0, and 3.0 mg/kg of the diet, in the form of sodium selenite (Na2SeO3)). Our results indicated that the HFD significantly increased the activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in the serum, as well as the degree of steatosis, the content of malondialdehyde (MDA), the apoptotic rate, and the level of mRNA caspase-3 in the liver compared to their BD counterparts (p < 0.05). Moreover, these parameters in the HFD groups were more significantly reduced (p < 0.05) for a Se concentration of 1.0 mg/kg than for the other concentrations. Further, for both the BD and HFD, the groups supplemented with 1.0 mg/kg Se showed the highest mRNA level of selenoprotein S. In conclusion, the consumption of an HFD can induce oxidative damage and apoptosis in the liver. This shows that the supplementation of Se at 1.0 mg/kg may be the optimum concentration against damage induced by HFD, and Sels may play a key role in this process.
Highlights
In the last two or three decades, nonalcoholic fatty liver disease (NAFLD) has become increasingly prevalent in many countries worldwide, as people continue to eat excessive dietary fat [1]
The pathological processes of NAFLD start with a fatty liver only and transition to nonalcoholic steatohepatitis (NASH) and, cirrhosis [2]
The objective of our study was to investigate the intervention of selenium in the high-fat-diet-induced oxidative stress and apoptosis of pig livers and the effects of four endoplasmic reticulum (ER)-resident selenoproteins in this process
Summary
In the last two or three decades, nonalcoholic fatty liver disease (NAFLD) has become increasingly prevalent in many countries worldwide, as people continue to eat excessive dietary fat [1]. The pathological processes of NAFLD start with a fatty liver only (steatosis) and transition to nonalcoholic steatohepatitis (NASH) and, cirrhosis [2]. A “two-hit” NASH pathogenesis model was proposed by Day (1998), who considered fat accumulation as the first hit and increased oxidative stress as the significant second hit [3]. The chronic intake of a high-fat diet (HFD) can abnormally increase hepatic triglyceride and cholesterol levels, potentially promoting lipid peroxidation and oxidative stress within hepatocytes [4]. Chronic oxidative stress that is mainly induced by mitochondrial dysfunction can develop into NAFLD and metabolic syndrome [5]. Oxidative stress can intervene in the functional expression of the proapoptotic signal protein genes of
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