Search

The nutritional status experienced in the early development of life plays a vital role in the long-term metabolic state of the individual, which is known as nutritional programming. The present study investigated the long-term effects of vegetable oil (VO) nutritional programming during the early life of large yellow croaker. First, larvae were fed either a fish oil (FO) diet or a VO diet for 30 d. Subsequently, under the same conditions, all fish were fed a commercial diet for 90 d and thereafter challenged with an FO or VO diet for 30 d. The results showed that growth performance was significantly lower in larvae fed the VO diet than in those in fed the FO diet in the stimulus phase. Notably, VO nutritional history fish showed lower levels of liver lipids liver total triglycerides and serum nonesterified free fatty acids than the FO nutritional history fish when juveniles were challenged with the VO diet, which was consistent with the expression of lipogenesis-related genes and proteins. Moreover, the VO nutritional history fish showed lower liver damage and higher antioxidant capacity than FO nutritional history fish when challenged with the VO diet. In summary, this study showed that a short VO stimulus during the early life stage of large yellow croaker, had a long-term effect on lipid metabolism and the antioxidant system. Specifically, VO nutritional programming had a positive effect on alleviating abnormal lipid deposition on the liver, liver damage, and the reduction of hepatic antioxidant capacity caused by a VO diet. [ABSTRACT FROM AUTHOR]

We investigated the role of zinc‐finger protein 281 (ZNF281), a novel molecule, in ethanol‐induced hepatocyte senescence and uncovered the potential mechanism. Real‐time PCR, Western blot, immunofluorescence staining, and enzyme‐linked immunosorbent assay were performed to explore the role of ZNF281 in hepatocyte senescence. ZNF281 expression was upregulated in both alcohol‐fed mice livers and ethanol‐treated hepatocytes. Silence of ZNF281 in hepatocytes using siRNA mitigated ethanol‐caused decrease in cell viability and increased release of aspartate aminotransferase, alanine transaminase, and lactate dehydrogenase. ZNF281 siRNA reduced senescence‐associated β‐galactosidase‐positive cells under ethanol exposure, abolished cell cycle arrest at G0/G1 phase, and diminished senescence‐associated secretory phenotype and proinflammatory cytokines (IL‐1β and IL‐6) release. At molecular level, ZNF281 deficiency altered the expression profile of senescence‐associated proteins including p53, p21, p16, high mobility group AT‐hook 1, and phospho‐histone H2A.X and telomerase‐associated regulatory factors including telomerase reverse transcriptase, telomeric repeat binding factor 1 (TRF1), and TRF2. ZNF281 knockdown promoted hepatocyte recovery from ethanol‐induced mitochondrial dysfunction and ROS production, which was correlated with rescuing HK2‐PINK1/Parkin signalling‐mediated mitophagy. Mechanistically, ZNF281 directly bound to 5′‐GGCGGCGGGCGG‐3′ motif within HK2 promoter region and transcriptionally repressed HK2 expression. Systematic ZNF281 knockdown by adeno‐associated virus encoding ZNF281 shRNA protected mice from alcohol feeding‐caused hepatocyte injury and senescence. This study provides a novel factor ZNF281 as a driver of hepatocyte senescence during alcoholic liver disease. [ABSTRACT FROM AUTHOR]

The high‐quality 3D model is the key to digital twin and visualization. Here, the neural radiation field (NeRF) is applied to greatly improve the speed and accuracy of 3D reconstruction of large‐scale substation equipment. The incremental SFM algorithm is used to accurately position the camera in open scenes, and the frame extraction experiment indicates that the single angle increment should not be greater than 8°. The reconstruction test is carried out on the power transformer and high‐voltage experimental equipment following the circular shooting track for instant‐NGP (a variant of NeRF). Compared with the traditional 3D reconstruction method, the speed of reconstruction is accelerated by 23–55 times, and the fidelity is improved by 2–3 times. Also, the deployment scheme of NeRF in the digital twin technology of large‐scale substation equipment is proposed. The experimental results verify the effectiveness and feasibility of NeRF in practical application. [ABSTRACT FROM AUTHOR]

Dietary l-carnitine (LC) is a nutritional factor that reduces liver lipid content. However, whether dietary LC can improve lipid metabolism via simultaneous activation of mitochondrial fatty acid (FA) β -oxidation and suppression of endoplasmic reticulum (ER) stress is still unknown. Large yellow croaker were fed with a high-fat diet (HFD) supplemented with dietary LC at 0, 1·2 or 2·4 ‰ for 10 weeks. The results indicated that a HFD supplemented with LC reduced the liver total lipid and TAG content and improved serum lipid profiles. LC supplementation administered to this fish increased the liver antioxidant capacity by decreasing serum and liver malondialdehyde levels and enhancing the liver antioxidant capacity, which then relieved the liver damage. Dietary LC increased the ATP dynamic process and mitochondrial number, decreased mitochondrial DNA damage and enhanced the protein expression of mitochondrial β -oxidation, biogenesis and mitophagy. Furthermore, dietary LC supplementation increased the expression of genes and proteins related to peroxisomal β -oxidation and biogenesis. Interestingly, feeding fish with LC-enriched diets decreased the protein levels indicative of ER stress, such as glucose-regulated protein 78, p-eukaryotic translational initiation factor 2a and activating transcription factor 6. Dietary LC supplementation downregulated mRNA expression relative to FA synthesis, reduced liver lipid and relieved liver damage through regulating β -oxidation and biogenesis of mitochondria and peroxisomes, as well as the ER stress pathway in fish fed with HFD. The present study provides the first evidence that dietary LC can improve lipid metabolism via simultaneously promoting FA β -oxidation capability and suppressing the ER stress pathway in fish. [ABSTRACT FROM AUTHOR]

A 30-d feeding trial was conducted to investigate effects of dietary eucommia ulmoides leaf extract (ELE) on growth performance, activities of digestive enzymes, antioxidant capacity, immunity, expression of inflammatory factors and feeding-related genes of large yellow croaker larvae. Five micro-diets were formulated with supplementation of 0 g kg−1 (the control), 5 g kg−1 (0·5 %), 10 g kg−1 (1·0 %) and 20 g kg−1 (2·0 %) of ELE, respectively. Results showed that the best growth performance was found in larvae fed the diet with 1·0 % ELE. Furthermore, ELE supplementation significantly increased the npy expression at 1·0 % dosage, while increased ghrelin in larvae at 0·5 % dosages. The activity of leucine aminopeptidase in larvae fed the diet with 1·0 % ELE was significantly higher than the control, while alkaline phosphatase was significantly upregulated in larvae fed the diet with 2·0 % ELE. A clear increase in total antioxidant capacity in larvae fed the diet with 1·0 % ELE was observed, whereas catalase activity was significantly higher in 1·0 % and 2·0 % ELE supplementation compared with the control. Larvae fed the diet with 1·0 % ELE had a significantly higher activities of lysozyme, total nitric oxide synthase and nitric oxide content than the control. Moreover, transcriptional levels of cox-2, il-1β and il-6 were remarkably downregulated by the supplementation of 0·5–1·0 % ELE. This study demonstrated that the supplementation of 1·0 % ELE in diet could increase the growth performance of large yellow croaker larvae probably by promoting expression of feeding-related genes, enhancing antioxidant capacity and immunity and inhibiting expression of inflammatory factors. [ABSTRACT FROM AUTHOR]

The [2+2] cycloaddition of allenes with alkenes is of much interest and importance as a straightforward route for the construction of four‐membered carbocycles but has remained much underexplored to date. Herein we report for the first time the intermolecular regio‐ and diastereoselective formal [2+2] cycloaddition of a wide range of allenes with amino‐functionalized alkenes by half‐sandwich rare‐earth catalysts. The reaction proceeded through an allene C(sp2)−H activation mechanism initiated by the site‐selective deprotonation of the allene unit by a rare‐earth metal alkyl species followed by alkene insertion into the resulting metal‐allenyl bond and the subsequent intramolecular cycloaddition to an allene C=C bond. This protocol offers a unique route for the synthesis of a new family of cyclobutane and cyclobutene derivatives which were difficult to access previously. [ABSTRACT FROM AUTHOR]