Scope
Punicalagin (PU)‐rich pomegranate peel extract has been shown before to exert protective effects against high fat‐induced hepatic damage. The aim of this study is to explore whether and how PU antagonizes hepatic steatosis in Western diet‐fed (WD) mice.
Methods and Results
Mice are fed either chow diet, WD (containing 42% fat, 15% protein, and 43% carbohydrates), or WD supplemented with PU (50 mg kg−1 body weight/day) for 13 weeks. Weight gain, hepatic fat content, and inflammation in the liver and adipose tissues are measured. Compared to the WD group, PU‐treated mice have lower fat content, decreased levels of alanine transaminase, and inflammation in liver. PU also changed the transcriptional expression of important genes in fatty acid oxidation pathway and alleviated glucose intolerance. Furthermore, PU improved adiponectin signaling and lipid metabolism in visceral adipose tissue. Moreover, PU improved gut microbiota dysbiosis induced by WD and enhanced gut barrier function.
Conclusions
The findings suggest that PU improves hepatic steatosis induced by WD, in part through regulating lipid homeostasis and inflammation in liver and adipose tissue and restoring microbiota shift and impaired gut barrier function. Thus, PU can be potentially developed as a potential prevention strategy in combating nonalcoholic fatty liver disease.
Cronobacter sakazakii, an emerging foodborne pathogen that was isolated primarily from powdered infant formula, poses an important issue in food safety due to its high stress tolerance and pathogenicity. The Hpr (encoded by ptsH gene) has been shown to regulate carbon metabolism as well as stress response and virulence. However, the functional properties of ptsH in C. sakzakii have not been investigated. In this study, we clarified the role of ptsH in the C. sakzakii stress response and virulence, and explored its possible regulatory mechanism by RNA-seq. Compared with wild-type, the ΔptsH mutant showed a slower growth rate in the log phase but no difference in the stationary phase. Moreover, the resistance to heat stress (65 °C, 55 °C), simulated gastric fluid (pH = 2.5), biofilm formation and adhesion to HT-29 cells of ΔptsH mutant were significantly decreased, whereas the oxidative resistance (1, 5, 10 mM H2O2), osmotic resistance (10%, 15%, 20% NaCl), and superoxide dismutase activity were enhanced. Finally, RNA-seq analysis revealed the sulfur metabolism pathway is significantly upregulated in the ΔptsH mutant, but the bacterial secretion system pathway is dramatically downregulated. The qRT-PCR assay further demonstrated that the ΔptsH mutant has elevated levels of genes that are related to oxidative and osmotic stress (sodA, rpoS, cpxA/R, osmY). This study provides a great understanding of the role of ptsH in diverse stress responses and virulence in C. sakazakii, and it contributes to our understanding of the genetic determinant of stress resistance and pathogenicity of this important foodborne pathogen.
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