Summary The objective of this study was to investigate the effect of mixed kojis on essential indices of fish sauce. Fish sauce inoculated with mixed kojis (FSB, Aspergillus oryzae koji:Aspergillus niger koji = 3:1) and A. oryzae koji (FSA, control) was prepared. At the end of fermentation, the content of amino nitrogen, total soluble nitrogen, Free amino acid (FAA) and glutamic acid in FSB increased by 7.50%, 7.84%, 9.80% and 28.43% compared to FSA, due to higher acid protease activity in mixed kojis. Moreover, flavour groups including phenols, ketones and nitrogen‐containing compounds in FSB were also improved. According to the results of sensory evaluation, FSB showed higher intensity of umami and caramel attributes, lower intensity of ammonia and sour attributes. All the results suggested that the usage of mixed kojis to produce fish sauce was an effective method that can accelerate the fermentation process and improve the flavour of fish sauce made with freshwater fish by‐products.

Selenium is recognized as an essential element for human health and enters human body mainly via diet. Selenium is a key constituent in selenoproteins, which exert essential biological functions, including antioxidant and anti-inflammatory effects. Several selenoproteins including glutathione peroxidases, selenoprotein P and selenoprotein S are known to play roles in the regulation of type 2 diabetes. Although there is a close association between certain selenoproteins with glucose metabolism or insulin resistance, the relationship between selenium and type 2 diabetes is complex and remains uncertain. Here we review recent advances in the field with an emphasis on roles of selenium on metabolism and type 2 diabetes. Understanding the association between selenium and type 2 diabetes is important for developing clinical practice guidelines, establishing and implementing effective public health policies, and ultimately combating relative health issues.

Background and Aims: NASH has emerged as a leading cause of chronic liver disease. However, the mechanisms that govern NASH fibrosis remain largely unknown. CREBZF is a CREB/ATF bZIP transcription factor that causes hepatic steatosis and metabolic defects in obesity. Approach and Results: Here, we show that CREBZF is a key mechanism of liver fibrosis checkpoint that promotes hepatocyte injury and exacerbates diet-induced NASH in mice. CREBZF deficiency attenuated liver injury, fibrosis, and inflammation in diet-induced mouse models of NASH. CREBZF increases HSC activation and fibrosis in a hepatocyte-autonomous manner by stimulating an extracellular matrix protein osteopontin, a key regulator of fibrosis. The inhibition of miR-6964-3p mediates CREBZF-induced production and secretion of osteopontin in hepatocytes. Adeno-associated virus –mediated rescue of osteopontin restored HSC activation, liver fibrosis, and NASH progression in CREBZF-deficient mice. Importantly, expression levels of CREBZF are increased in livers of diet-induced NASH mouse models and humans with NASH. Conclusions: Osteopontin signaling by CREBZF represents a previously unrecognized intrahepatic mechanism that triggers liver fibrosis and contributes to the severity of NASH.