Differences in the anti-hyperuricemic and anti-inflammation effects between two sea cucumber hydrolysates in diet induced hyperuricemic mice.

Recently, interest in using whole food‐derived mixtures to alleviate chronic metabolic syndrome through potential synergistic interactions among different components is increasing. In this study, the effects and mechanisms of tuna meat oligopeptides (TMOP) on hyperuricemia and associated renal inflammation were investigated in mice. Dietary administration of TMOP alleviated hyperuricemia and renal inflammation phenotypes, reprogramed uric acid metabolism pathways, inhibited the activation of NLRP3 inflammasome and TLR4/MyD88/NF‐κB signaling pathways, and suppressed the phosphorylation of p65‐NF‐κB. In addition, TMOP treatments repaired the intestinal epithelial barrier, reversed the gut microbiota dysbiosis and increased the production of short‐chain fatty acids. Moreover, the antihyperuricemia effects of TMOP were transmissible by transplanting the fecal microbiota from TMOP‐treated mice, indicating that the protective effects were at least partially mediated by the gut microbiota. Thus, for the first time, we clarify the potential effects of TMOP as a whole food derived ingredient on alleviating hyperuricemia and renal inflammation in mice, and additional efforts are needed to confirm the beneficial effects of TMOP on humans.

Scope The effects and mechanism of tuna bone powder (TBP) on glucocorticoid‐induced osteoporosis (GIOP) alleviation in terms of signaling pathway coregulation and gut microbiota modulation are investigated. Methods and results The powder size distribution and composition of TBP are measured. The GIOP female mice induced by dexamethasone intramuscular injection are used to examine the anti‐osteoporosis effects of TBP in a 10 week experiment, and improved bone mineral density and bone microarchitecture are observed via micro‐CT. In addition, qRT‐PCR results show that the NF‐κB pathway is inhibited to reduce bone resorption, whereas the Wnt/β‐catenin pathway is activated to enhance bone formation after treatment. Moreover, TBP treatments suppress the release of pro‐inflammatory cytokines, repair dysfunction of the intestinal epithelial barrier, and prevent aggravated systemic inflammation in mRNA levels. Additionally, 16S rRNA gene sequencing indicate that TBP treatments enhance the abundance of anti‐inflammatory bacteria and short‐chain fatty acid (SCFA) producers, which is consistent with increased SCFA contents in feces measured via GC–MS. Conclusion These data show that TBP ameliorates GIOP in mice through four aspects, including coregulating signaling pathways, blocking proinflammatory cytokines, repairing the intestinal epithelial barrier, and modulating gut microbiota. Therefore, TBP may be a potential prebiotic agent to alleviate osteoporosis in humans.

Obesity has become a worldwide epidemic. According to a report, more than 2.1 billion people have a body mass index ≥25.0 and ≥30.0, and more than half a billion of them with no distinction of age or sex worldwide (Jérôme et al., 2019). This increasing prevalence has become a global health concern and is causing a substantial socioeconomic burden. Obesity, characterized by fat accumulation,

Hyperuricaemia is a disease associated with elevated serum uric acid content, which has emerged rapidly in recent decades. The drugs used to treat clinical hyperuricaemia have side effects, and their...