Fructose induces hepatic steatosis in adolescent mice linked to the disorders of lipid metabolism, bile acid metabolism, and autophagy.

The effects of excessive fructose intake on the development and progression of metabolic disorders have received widespread attention. However, the deleterious effects of fructose on the development of hepatic metabolic disease in adolescents and its potential mechanisms are not fully understood. In this study, we investigated the effects of isocaloric fructose-rich diets on the liver of adolescent mice. The results showed that fructose-rich diets had no effect on the development of obesity in the adolescent mice, but did induce hepatic lipid accumulation. Besides, we found that fructose-rich diets promoted hepatic inflammatory responses and oxidative stress in adolescent mice, which may be associated with activation of the NLRP3 inflammasome and inhibition of the Nrf2 pathway. Furthermore, our results showed that fructose-rich diets caused disturbances in hepatic lipid metabolism and bile acid metabolism, as well as endoplasmic reticulum stress and autophagy dysfunction. Finally, we found that the intestinal barrier function was impaired in the mice fed fructose-rich diets. In conclusion, our study demonstrates that dietary high fructose induces hepatic metabolic disorders in adolescent mice. These findings provide a theoretical foundation for fully understanding the effects of high fructose intake on the development of hepatic metabolic diseases during adolescence.

Anti-UV Microgel Based on Interfacial Polymerization to Decrease Skin Irritation of High Permeability UV Absorber Ethylhexyl Methoxycinnamate.

Ethylhexyl methoxycinnamate (EHMC) is frequently employed as a photoprotective agent in sunscreen formulations. EHMC has been found to potentially contribute to health complications as a result of its propensity to produce irritation and permeate the skin. A microgel carrier, consisting of poly(ethylene glycol dimethacrylate) (pEDGMA), was synthesized using interfacial polymerization with the aim of reducing the irritation and penetration of EHMC. The thermogravimetric analysis (TGA) indicated that the EHMC content accounted for 75.72% of the total composition. Additionally, the scanning electron microscopy (SEM) images depicted the microgel as exhibiting a spherical morphology. In this study, the loading of EHMC was demonstrated through FTIR and contact angle tests. The UV resistance, penetration, and skin irritation of the EHMC-pEDGMA microgel were additionally assessed. The investigation revealed that the novel sunscreen compound, characterized by limited dermal absorption, had no irritant effects and offered sufficient protection against ultraviolet radiation.

Removal of leftover feed shapes environmental microbiota and limits houseflies-mediated dispersion of pathogenic bacteria in sow breeding farms.

BACKGROUND: Intensive swine breeding industry generates a complex environment where several microbial interactions occur and which constitutes a challenge for biosafety. Ad libitum feeding strategies and low levels of management contribute to residual and wasted feed for lactating sows, which provides a source of nutrients and microbial source for houseflies in warm climates. Due to the absence of the all-in/all-out system, the coexistence of sows of two production stages including gestating and lactating sows in the farrowing barn may have potential negative impacts. In this research, we evaluated the effects of lactating sow leftover on the environmental microbiota of the farrowing barn and the contribution of microbial environments to the gestating sow fecal bacterial structure with a 30-day-long treatment of timely removing lactating residual feed. RESULTS: Houseflies in the farrowing barn mediate the transmission of microorganisms from lactating sow leftover to multiple regions. Leuconostoc, Weissella, Lactobacillus and Pediococcus from the leftover which can produce exopolysaccharides, are more capable of environmental transmission than pathogenic microorganisms including Staphylococcus and Streptococcus and utilize houseflies to achieve spread in environmental regions of the farrowing barn. Leftover removal treatment blocked the microbial transmission chain mediated by houseflies, downregulated the relative abundance of pathogenic bacteria including Escherichia-Shigella and Streptococcus among houseflies, environmental regions and fecal bacteria of gestating sows in the farrowing barn and effectively attenuate the increment of Weissella and RF39 relative abundance in gestating sow feces due to the presence of lactating sows. CONCLUSIONS: Lactating sow leftover is a non-negligible microbial contributor of environment in farrowing barn whose transmission is mediated by houseflies. A 30-day-long treatment of removing lactating sow residual feed cause significant changes in the microbial structure of multiple environmental regions within the farrowing barn via altering the microbiota carried by houseflies. Meanwhile, lactating sow leftover affect the fecal microbial structure of gestating sows in the same farrowing barn, while removal of lactating sow leftover alleviates the contribution of microbial transmission.

Network Pharmacology, Molecular Docking, and Experimental Verification to Reveal the Mitophagy-Associated Mechanism of Tangshen Formula in the Treatment of Diabetic Nephropathy.

Purpose: This study investigated the mechanism of TSF in treating DN through network pharmacology, molecular docking, and experimental validation. Methods: To identify critical active ingredients, targets, and DN genes in TSF, multiple databases were utilized for screening purposes. The drug-compound-target network was constructed using Cytoscape 3.9.1 software for network topological analysis. The protein interaction relationship was analyzed using the String database platform. Metascape database conducted enrichment analysis on the key targets using Gene Ontology and the Kyoto Encyclopedia of Genes and Genomes. The renoprotective effect was evaluated using a mouse model of diabetic nephropathy (db/db mice) that occurred spontaneously. Validation of the associated targets and pathways was performed using Western Blot (WB), Polymerase Chain Reaction (PCR), and Immunohistochemical methods (IHC). Results: The network analysis showed that the TSF pathway network targeted 24 important targets and 149 significant pathways. TSF might have an impact by focusing on essential objectives such as TP53, PTEN, AKT1, BCL2, BCL2L1, PINK-1, PARKIN, LC3B, and NFE2L2, along with various growth-inducing routes. Our findings demonstrated that TSF effectively repaired the structure of mitochondria in db/db mice. TSF greatly enhanced the mRNA levels of PINK-1. WB and IHC findings indicated that TSF had a notable impact on activating the PINK-1/PARKIN signaling pathway in db/db mice, significantly increasing LC3 and NRF2 expression. Conclusion: Our results indicate that TSF effectively addresses DN by activating the PINK-1/PARKIN signaling pathway and enhancing Mitochondrion structure in experimental diabetic nephropathy.