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Patients with type 2 diabetes mellitus (T2DM) are more susceptible to acute myocardial ischemia/reperfusion (MI/R) injury. However, the mechanism remains largely elusive. Clinical observation showed that high levels of hepatokine fetuin-B (FetB) in plasma are significantly associated with both diabetes and coronary artery diseases. This study was aimed to determine whether FetB mostly derived from liver exacerbates MI/R-induced injury and the underlying mechanisms in T2DM. Mice were given high-fat diet and streptozotocin to induce T2DM model and subjected to 30 min MI followed by reperfusion. Diabetes caused increased hepatic FetB expression and greater myocardial injury as evidenced by increased apoptosis and myocardial enzymes release following MI/R. In T2DM hearts, insulin-induced phosphorylations of insulin receptor substrate 1 at Tyr608 site and Akt at Ser473 site and glucose transporter 4 membrane translocation were markedly reduced. Interaction between FetB and insulin receptor-β subunit (IRβ) was enhanced assessed by immunoprecipitation analysis. More importantly, FetB knockdown via AAV9 alleviated MI/R injury and improved cardiac insulin-induced signaling in T2DM mice. Conversely, upregulation of FetB in normal mice caused exacerbated MI/R injury and impairment of insulin-mediated signaling. In cultured neonatal mouse cardiomyocytes, incubation of FetB significantly reduced tyrosine kinase activity of IR and insulin-induced glucose uptake, and increased hypoxia/reoxygenation-induced apoptosis. Furthermore, FoxO1 knockdown by siRNA suppressed FetB expressions in hepatocytes treated with palmitic acid. In conclusion, upregulated FetB in diabetic liver contributes to increased MI/R injury and cardiac dysfunction via directly interacting with IRβ and consequently impairing cardiac insulin signaling. • Hepatokine fetuin-B is significantly upregulated in diabetes. • Upregulated fetuin-B exacerbates MI/R injury in diabetes and suppression of fetuin-B exerts cardiac protective effects. • Fetuin-B interacts with insulin receptor-β subunit, impairs cardiac insulin signaling and consequently causes MI/R injury. [ABSTRACT FROM AUTHOR]

The present study investigated the effect of ε-Polylysine on bacterial communities, sensorial, and chemical properties [total volatile basic nitrogen (TVB-N), biogenic amines, and breakdown products of adenosine triphosphate] of bighead carp ( Aristichthys nobilis ) fillets stored at 4 ± 1 °C. Bacterial communities were explored by the culture-dependent method and the high-throughput sequencing targeting on 16S rRNA genes. The results showed that the major genera in spoiled control samples were Aeromonas , Pseudomonas , Shewanella , and Acinetobacter . ε-Polylysine inhibited the growth of Pseudomonas , Shewanella , and Acinetobacter . Consequently, Aeromonas and Janthinobacterium were dominant in spoiled treated samples. The sensorial shelf-life of the control and treated groups were 8 days and 10 days, respectively. Furthermore, due to the inhibitory effect of ε-Polylysine on bacteria, chemical changes of the treated group were slower, reflecting as lower concentrations of TVB-N, putrescine, cadaverine, and hypoxanthine, and higher contents of inosine 5′-monophosphate and hypoxanthine riboside at the end of storage. In conclusion, ε-Polylysine altered the bacterial communities and delayed quality deterioration of bighead carp fillets during chilled storage. [ABSTRACT FROM AUTHOR]