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Hepatic steatosis is the most common phenomenon of lipid metabolism disorder in farmed fish, but its molecular mechanism is poorly understood. Therefore, the present study was aimed to investigate hepatic steatosis induced by high-fat diet (HFD) and explore underlying mechanism in tilapia. The fish were fed on control diet or HFD for 90 days. The blood and liver tissues were collected to determine biochemical parameter, gene expression and protein level after 30, 60, and 90 days, and analyzed lipid accumulation, endoplasmic reticulum (ER) stress and autophagy. After 30 days of feeding, the plasmatic and hepatic lipid content (TG, TCH, LDL-C, and HDL-C) and fatty acid (FA) transportation (fabp1 and CD36) were enhanced significantly in HFD-fed tilapia. After 60 days, HFD feeding increased TG synthesis and free CH formation, and decreased FAs β-oxidation and biosynthesis in liver of tilapia. Further, with increasing lipid accumulation, ER stress was induced, which worsened hepatic steatosis via activating IRE1 signaling pathway in liver of HFD group after 90 days. Meanwhile, HFD feeding suppressed autophagy via impairing AMPK and TFEB pathways in tilapia liver after 90 days. Our results demonstrated that HFD feeding induced extensive lipid deposition, promoted ER stress, suppressed autophagy in tilapia liver. Interestingly, these pathological features were positively correlated with the duration of HFD feeding.

Abstract Diffusion is an important mass transfer mode of tight sandstone gas. Since nano-pores are extensively developed in the interior of tight sandstone, a considerable body of research indicates that the type of diffusion is mainly molecular diffusion based on Fick’s law. However, accurate modeling and understanding the physics of gas transport phenomena in nano-porous media is still a challenge for researchers and traditional investigation (analytical and experimental methods) have many limitations in studying the generic behavior. In this paper, we used Nano-CT to observe the pore structures of samples of the tight sandstone of western of Sichuan. Combined with advanced image processing technology, three-dimensional distributions of the nanometer-sized pores were reconstructed and a tight sandstone digital core model was built, as well the pore structure parameters were analyzed quantitatively. Based on the digital core model, the diffusion process of methane molecules from a higher concentration area to a lower concentration area was simulated by a finite volume method. Finally, the reservoir’s concentration evolution was visualized and the intrinsic molecular diffusivity tensor which reflects the diffusion capabilities of this rock was calculated. Through comparisons, we found that our calculated result was in good agreement with other empirical results. This study provides a new research method for tight sandstone digital rock physics. It is a foundation for future tight sandstone gas percolation theory and numerical simulation research.

Tilapia is susceptible to hepatic steatosis when grown in intensive farming systems. The aim of this study was to explore the mechanism of fatty liver induced by a high-fat diet (HFD) in genetically improved farmed tilapia (GIFT, Oreochromis niloticus). Juvenile GIFT were fed with HFD or a normal-fat diet (NFD) for 60 days. Substantial fat deposition in the liver of HFD-fed GIFT on days 20, 40, and 60 was observed using hematoxylin – eosin staining and oil red O staining. The increased fat deposition was consistent with increased triglyceride (TG) and total cholesterol (TC) levels in the liver of HFD-fed GIFT. There were significant differences (P < 0.05) in serum biochemical indexes (TG, TC, low density lipoprotein-cholesterol, and insulin contents, and alanine aminotransferase activity) between GIFT fed a HFD and GIFT fed a NFD on days 20, 40, and 60. Furthermore, 60 days of a HFD significantly changed (P < 0.05) the hepatic fatty acid composition, and led to increased polyunsaturated fatty acid levels and decreased saturated fatty acid and monounsaturated fatty acid levels. Hepatic antioxidant enzyme activities increased by day 20 and then declined, which led to an increase in malondialdehyde contents in the liver of HFD-fed GIFT. Molecular analyses revealed that the microRNAs miR-122, miR-29a, and miR-145-5p were upregulated, whereas miR-34a was downregulated in HFD-fed GIFT. SCD, ELOVL6, and SRD5A2 encode three important enzymes in lipid metabolism, and were identified as potential targets of miRNAs. The transcript levels of hepatic SCD and ELOVL6 were decreased and that of hepatic SRD5A2 was increased in GIFT fed a HFD. Overall, the results of this study revealed a potential link between miRNAs and fatty liver induced by HFD, and suggest that a HFD could lead to excess fat deposition in the GIFT liver, which may disrupt hepatic lipid metabolism and reduce the antioxidant defense capacity.

Tilapia is susceptible to hepatic steatosis when grown in intensive farming systems. The aim of this study was to explore the mechanism of fatty liver induced by a high-fat diet (HFD) in genetically improved farmed tilapia (GIFT, Oreochromis niloticus). Juvenile GIFT were fed with HFD or a normal-fat diet (NFD) for 60 days. Substantial fat deposition in the liver of HFD-fed GIFT on days 20, 40, and 60 was observed using hematoxylin – eosin staining and oil red O staining. The increased fat deposition was consistent with increased triglyceride (TG) and total cholesterol (TC) levels in the liver of HFD-fed GIFT. There were significant differences (P < 0.05) in serum biochemical indexes (TG, TC, low density lipoprotein-cholesterol, and insulin contents, and alanine aminotransferase activity) between GIFT fed a HFD and GIFT fed a NFD on days 20, 40, and 60. Furthermore, 60 days of a HFD significantly changed (P < 0.05) the hepatic fatty acid composition, and led to increased polyunsaturated fatty acid levels and decreased saturated fatty acid and monounsaturated fatty acid levels. Hepatic antioxidant enzyme activities increased by day 20 and then declined, which led to an increase in malondialdehyde contents in the liver of HFD-fed GIFT. Molecular analyses revealed that the microRNAs miR-122, miR-29a, and miR-145-5p were upregulated, whereas miR-34a was downregulated in HFD-fed GIFT. SCD, ELOVL6, and SRD5A2 encode three important enzymes in lipid metabolism, and were identified as potential targets of miRNAs. The transcript levels of hepatic SCD and ELOVL6 were decreased and that of hepatic SRD5A2 was increased in GIFT fed a HFD. Overall, the results of this study revealed a potential link between miRNAs and fatty liver induced by HFD, and suggest that a HFD could lead to excess fat deposition in the GIFT liver, which may disrupt hepatic lipid metabolism and reduce the antioxidant defense capacity. [ABSTRACT FROM AUTHOR]