Cherry juice alleviates high-fat diet-induced obesity in C57BL/6J mice by resolving gut microbiota dysbiosis and regulating microRNA.

Cherry is a nutrient-rich food that is good for health. This study demonstrated the inhibitory action of dietary cherry juice on high-fat diet (HFD)-induced obesity in mice. Cherry juice intervention significantly decreased body weight, fat contents, and blood lipid levels in obese mice. The overproduction of proinflammatory cytokines was suppressed by dietary cherry juice, which was accompanied by the elevation of tight junction proteins to maintain intestinal barrier. Moreover, dietary cherry juice restored the decreased production of short-chain fatty acids (SCFAs) by regulating the composition and abundance of gut microbiota. In addition, dietary cherry juice also suppressed the expression of some microRNAs associated with obesity such as miR-200c-3p, miR-125a-5p, miR-132-3p, and miR-223-3p and target proteins related with microRNAs in the inguinal or epididymal white tissue in the obese mice. These results offer a fresh perspective on cherry juice's role in the prevention of obesity caused by the HFD.

Dietary Acrylamide Intake Alters Gut Microbiota in Mice and Increases Its Susceptibility to Salmonella Typhimurium Infection.

Acrylamide (AA) has been extensively examined for its potential toxicological effects on humans and animals, but its impacts on gut microbiota and effects on hosts' susceptibility to enteric infection remain elusive. The present study was designed to evaluate the effect of AA on gut microbiota of mice and susceptibility of mice to S. Typhimurium infection. After four weeks' intervention, mice fed with AA exhibited significantly decreased body weight. Meanwhile, 16S rRNA gene sequencing showed reduced relative abundance of Firmicutes and increased abundance of Bacteroidetes in AA-treated mice prior to infection. In addition, we observed high relative abundance of Burkholderiales and Erysipelotrichales, more specifically the genus Sutterella and Allobaculum, respectively, in AA-treated mice before infection. Subsequently, the mice were orally infected with S. Typhimurium. The histological changes, systemic dissemination of S. Typhimurium, and inflammatory responses were examined. Compared to mice fed with normal diet, mice fed AA exhibited higher level of bacterial counts in liver, spleen, and ileum, which was consistent with exacerbated tissue damage determined by histological analyses. In addition, higher expression of pro-inflammaroty cytokines, p-IκBα, and p-P65 and lower mRNA expressions of mucin2, occludin, zo-1, claudin-1, and E-cadherin were detected in AA-treated mice. These findings provide novel insights into the potential health impact of AA consumption and the detailed mechanism for its effect on S. Typhimurium infection merit further exploration.

Fish oil extracted from Coregonus peled improves obese phenotype and changes gut microbiota in a high-fat diet-induced mouse model of recurrent obesity.

Recurrent obesity is rapidly emerging as a public health problem. Previous studies have confirmed that fish oil supplementation can alleviate obesity in mice; however, the effect of fish oil on recurrent obesity remains unclear. In the present study, the modulatory effects of fish oil extracted from Coregonus peled on the phenotypes and gut microbiota of recurrent obese mice were evaluated by MRI, OGTT, and bioinformatics analysis. We found that fish oil supplementation could significantly reduce the body weight gain, net weight gain, body fat distribution, and glucose tolerance. In addition, the composition and structure of gut microbiota were significantly shifted toward those of the control group by fish oil treatment. Moreover, the relative abundance of gut microbiota, such as Bacteroidetes, Bacteroidia, Lachnospiraceae, and Bifidobacterium, was markedly responding to the rapid dietary changes between fish oil and high-fat diet. Overall, our results confirmed that the alleviation of recurrent obesity using fish oil supplementation might be modulated by altering the hysteretic behavior and memory-like function of gut microbiota. We proposed that further studies are needed to elucidate the modulation mechanism.