Selenium improved mitochondrial quality and energy supply in the liver of high-fat diet-fed grass carp (Ctenopharyngodon idella) after heat stress.

This study aims to explore the effects of dietary selenium on hepatic mitochondrial quality and energy supply of grass carp (Ctenopharyngodon idella) fed with high-fat diet (HFD) after heat stress (HS). Grass carp were fed with HFD, and HFD contained 0.3 mg/kg nano-selenium for 10 weeks, thereafter exposed to HS from 26 to 34 °C, and named the HFD + HS (control) group and the HFD + Se + HS group, respectively. The results show that selenium significantly prompted the growth, increased glutathione peroxidase (GPX) activity, but reduced malondialdehyde (MDA) content in the liver and the levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in the serum of grass carp fed with HFD after HS. Further, selenium alleviated mitochondrial damage and increased the number of mitochondrial DNA copies in the liver of the grass carp fed with HFD after HS. And selenium also maintained mitochondrial homeostasis by upregulating the expression of mitochondrial quality control-related genes (pgc-1α, nrf1/2, tfam, opa1, mfn1/2, and drp1), mitophagy-related genes (beclin1, atg5, atg12, pink1, and parkin), and the protein expression of parkin and LC3-II/I in the liver of grass carp. Finally, selenium reduced the triglyceride (TG) level and increased the free fatty acid (FFA) level and adenosine triphosphate (ATP) production in the liver of grass carp fed with HFD after HS. In conclusion, dietary selenium alleviated liver damage and improved liver mitochondrial quality and ATP production by increasing liver antioxidant capacity and promoting liver mitochondrial quality in grass carp fed with HFD after HS, which help grass carp to resist these two stressors.

Selenium reduces hepatopancreas lipid accumulation of grass carp (Ctenopharyngodon idella) fed high-fat diet via lipophagy activation.

It has been reported that selenium (Se) can reduce hepatopancreas lipid accumulation induced by high-fat diet. However, its mechanism is still unknown. This study aims to investigate the specific mechanisms by which Se alleviates high-fat diet-induced lipid accumulation. Grass carp were fed control diet (4.8% lipid, Con), high-fat diet (8.8% lipid, HFD) or HFD supplemented with 0.3 mg/kg nano-Se (HSe0.3) for 10 weeks. Growth performance, Se deposition, lipid accumulation, hepatic ultrastructure, and gene and protein expression levels associated with autophagy were examined. Furthermore, oleic acid (OA) was used to incubate the grass carp hepatocytes (L8824) for 24 h, and then the L8824 were incubated with sodium selenite in presence or absence of an autophagy inhibitor for 24 h. L8824 was analyzed for triglyceride concentration, immunofluorescence, and gene and protein expression levels associated with autophagy. We found that dietary nano-Se improved the growth of fish fed HFD and also decreased hepatosomatic index and intraperitoneal fat ratio of fish fed HFD (P < 0.05). HFD significantly increased hepatopancreas lipid accumulation and decreased autophagic activity (P < 0.05). Treatment of grass carp fed HFD with nano-Se decreased lipid accumulation and restored hepatic autophagy (P < 0.05). In vitro, Se (100 µM sodium selenite) obviously activated autophagy in L8824 incubated with OA, and consequently reduced the lipid accumulation induced by OA (P < 0.05). Furthermore, using pharmacological inhibition (chloroquine) of the autophagy greatly diminished the beneficial effects of Se on alleviating OA-induced lipid accumulation and increased the co-localization of lipid droplets with autophagosome (P < 0.05), which indicated that Se increased autophagic flux. In conclusion, these results suggest that Se alleviates HFD-induced hepatopancreas lipid accumulation by activating lipophagy.

Seabuckthorn polysaccharide ameliorates high-fat diet-induced obesity by gut microbiota-SCFAs-liver axis.

Obesity has been reported to be associated with gut microbiome dysbiosis. seabuckthorn fruits have traditionally been used in Tibetan foods and medicines for thousands of years. Seabuckthorn polysaccharide (SP) is one of the main functional components in seabuckthorn fruits. However, the effects of SP on a high-fat diet (HFD)-induced obesity have not yet been elucidated. The purpose of this study is to explore the amelioration effect of SP on obesity induced by HFD and to reveal its mechanism of gut microbiota and its metabolites. Results showed that 12-week SP (0.1%, w/w) dietary supplementation could significantly reduce body weight gain, serum lipid level and liver triglycerides level in obese mice. Notably, the SP treatment elevated p-AMPKα and PPARα proteins expression stimulated the phosphorylation of ACC1 and inhibited the protein expression of FAS, PPARγ, and CD36 in the mice liver. Further, SP also reorganized the gut microbiome by up-regulating the proportion of Muribaculaceae_unclassified, Bifidobacterium, Rikenellaceae_RC9_gut_group, Alistipes, and Bacteroides, and down-regulating the abundance of Lactobacillus, Firmicutes_unclassified, Dubosiella Bilophila, and Streptococcus in HFD-induced obese mice. Moreover, the production of microbial metabolites short-chain fatty acids (SCFAs) in feces has also increased. In addition, correlation analysis results showed that obesity-ameliorating effects of SP were highly associated with levels of SCFAs in feces. Therefore, the regulation of SP on liver lipid metabolism may be due to the variation of the gut microbiome and raised production of SCFAs. These results indicate that SP could play the part of a potential nutraceutical for ameliorating obesity through regulation of the gut-liver axis.