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.

Isinglass Polysaccharides Regulate Intestinal-Barrier Function and Alleviate Obesity in High-Fat Diet Mice through the HO-1/Nrf2 Pathway and Intestinal Microbiome Environment.

Plant polysaccharide intervention has shown significant potential to combat obesity. However, studies on animal polysaccharides are indeed rare. The aim of this study was to investigate the potential functions of CIP (IL) on obesity, intestinal microflora dysbiosis, and the possible protection of intestinal barrier in mice fed with high-fat diet (HFD). Our results revealed that after 13 weeks, the HFD+L (high-fat diet + 25 mg/kg CIP) group showed significantly more weight loss and fat accumulation relative to the HFD+H (high-fat diet + 50 mg/kg CIP) group. Furthermore, CIP intervention modulated lipid metabolism and mRNA levels of inflammatory mediators in liver. Overall, CIP clearly improved the intestinal barrier in HFD-fed mice. Additionally, we observed that CIP intervention improved intestinal microbiota community richness and diversity in HFD-fed mice. The CIP intervention mice group showed a relatively low Firmicutes to Bacteroidetes ratio compared to the HFD group. This study concluded that CIP could be used as a functional food to prevent adipocyte accumulation, reduce systemic inflammation, and protect the intestinal barrier.

Jellyfish skin polysaccharides enhance intestinal barrier function and modulate the gut microbiota in mice with DSS-induced colitis.

Jellyfish skin polysaccharides (JSP) were isolated from Rhopilema esculentum Kishinouye and contained 55.11% polysaccharides and 2.26% uronic acid. To examine the anti-inflammatory, antioxidant and immunomodulatory activities of JSP in vivo, C57BL/6 mice were induced to develop ulcerative colitis by dextran sulfate sodium (DSS) and the roles of dietary JSP supplementation in modulating colitis were explored. JSP supplementation reduced the symptoms of colitis in mice, increased colon length, protected goblet cells, and improved intestinal epithelial integrity and permeability. JSP modulated oxidative stress and inflammatory responses, which was demonstrated by reduced MPO activity, NO level, and levels of pro-inflammatory cytokines including TNF-α, IL-1ß and IL-6 in mice. JSP suppressed NF-κB signaling pathways as evidenced by lower levels of phosphorylated p65 and IKB. Moreover, JSP supplementation enhanced the expression of tight junction proteins and mucins, and modulated the composition of the gut microbiota and the production of short-chain fatty acids. Taken together, these results reveal the anti-inflammatory effect of dietary JSP in vivo, suggesting the potential of JSP as a nutritional supplement or adjunct strategy in preventing or ameliorating colitis.

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.

Application of high-pressure homogenization for improving the physicochemical, functional and rheological properties of myofibrillar protein.

The present work investigated effects of high-pressure homogenization (HPH) pressure (0, 40, 80 and 120 MPa) on physicochemical, functional and rheological properties of clam myofibrillar protein (CMP). Results showed that HPH changed the CMP secondary and tertiary structures. Absolute zeta potential and protein solubility increased but particle size and turbidity of CMP decreased after HPH treatment. Both of emulsifying properties and foaming properties were significantly improved. The shear stress, apparent viscosity and the viscosity coefficients reduced, but flow index increased. Application of HPH improved the physicochemical, functional and rheological properties of CMP, and 120 MPa was the optimal pressure for modification.