Abstract
This study used 40 castrated male pigs to determine the protective effects of a new selenium molecule (hydroxy selenomethionine, OH-SeMet) on dietary oxidative stress (DOS) induced hepatic lipid metabolism disorder, and corresponding response of selenotranscriptome. The pigs were randomly grouped into 5 dietary treatments and fed a basal diet formulated with either normal corn and oils or oxidized diet in which the normal corn and oils were replaced by aged corn and oxidized oils, and supplemented with OH-SeMet at 0.0, 0.3, 0.6 and 0.9 mg Se/kg for a period of 16 weeks (n = 8). The results showed that DOS induced liver damage, increased serum alanine aminotransferase (ALT) and alkaline phosphatase (ALP) levels, decreased serum triacylglycerol (TG) level, suppressed antioxidant capacity in the liver, and changed lipid metabolism enzyme activity, thus causing lipid metabolism disorder in the liver. The DOS-induced lipid metabolism disorder was accompanied with endoplasmic reticulum (ER) stress, changes in lipid metabolism-related genes and selenotranscriptome in the liver. Dietary Se supplementation partially alleviated the negative impact of DOS on the lipid metabolism. These improvements were accompanied by increases in Se concentration, liver index, anti-oxidative capacity, selenotranscriptome especially 11 selenoprotein-encoding genes, and protein abundance of GPX1, GPX4 and SelS in the liver, as well as the decrease in SelF abundance. The Se supplementation also alleviated ER stress, restored liver lipid metabolism enzyme activity, increased the mRNA expression of lipid synthesis-related genes, and decreased the mRNA levels of lipidolysis-related genes. In conclusion, the dietary Se supplementation restored antioxidant capacity and mitigated ER stress induced by DOS, thus resisting hepatic lipid metabolism disorders that are associated with regulation of selenotranscriptome.
Highlights
The liver is the major metabolic organ in mammals, playing a crucial role in the metabolism of lipids
We found that the increased expressions of 11 selenoprotein-encoding genes were positively correlated with the expression of lipid synthesis-related genes under dietary oxidative stress (DOS), which is mainly reflected in increasing fatty acid synthetase (FASN), stearoyl-CoA desaturase (SCD) and sterol regulatory element binding protein 1c (SREBP1c) levels
The results of our study suggest the DOS induced liver damage leads to lipid
Summary
The liver is the major metabolic organ in mammals, playing a crucial role in the metabolism of lipids. Hepatic disorder in lipid metabolism is a major risk factor in many diseases, such as hyperlipemia and fatty liver disease [1]. The current leading theories posit that one of the main causes of abnormal lipid metabolism is oxidative stress (OS) [2,3], the regulation of OS on lipid metabolism is diverse under different physiological. Most published studies on lipid metabolism suggest that OS promotes production of reactive oxygen species and suppresses antioxidant capacity, causing liver injury and lipid accumulation [4,5]. Study manifests that OS attenuates lipid synthesis and facilitates β-oxidation in hepatoma cells [6]. The endoplasmic reticulum (ER) represents a complex membranous network that plays an important role in the lipid synthesis and transportation [7,8], and ER homeostasis is essential for lipid metabolism
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