Codium fragile (CF) is a functional seaweed food that has been used for its health effects, including immunostimulatory, anti-inflammatory, anti-obesity and anti-cancer activities, but the effect of CF extracts on obesity via regulation of intestinal microflora is still unknown. This study investigated anti-obesity effects of CF extracts on gut microbiota of diet-induced obese mice. C57BL/6 mice fed a high-fat (HF) diet were given CF extracts intragastrically for 12 weeks. CF extracts significantly decreased animal body weight and the size of adipocytes, while reducing serum levels of cholesterol and glucose. In addition, CF extracts significantly shifted the gut microbiota of mice by increasing the abundance of Bacteroidetes and decreasing the abundance of Verrucomicrobia species, in which the portion of beneficial bacteria (i.e., Ruminococcaceae, Lachnospiraceae and Acetatifactor) were increased. This resulted in shifting predicted intestinal metabolic pathways involved in regulating adipocytes (i.e., mevalonate metabolism), energy harvest (i.e., pyruvate fermentation and glycolysis), appetite (i.e., chorismate biosynthesis) and metabolic disorders (i.e., isoprene biosynthesis, urea metabolism, and peptidoglycan biosynthesis). In conclusion, our study showed that CF extracts ameliorate intestinal metabolism in HF-induced obese mice by modulating the gut microbiota.

Porphyra tenera (PT) is a functional seaweed food that has been reported for health benefits such as antioxidant, immunostimulant, anti-inflammation, and hepatoprotective effects. In this study, we investigated the effect of PT extracts on gut microbiota modulation in colitis-induced mice. The mice experiment was designed as three groups including normal mice (CTL), dextran sodium sulfate (DSS)-fed mice, and DSS plus PT extracts-fed mice (PTE). DSS was administrated through drinking water containing DSS for 1 week, and the PT extract was ingested into the gastrointestinal tract in mice. PT extract ameliorated the decreased body weight and colon length and improved disease activity index and pro-inflammatory cytokine expression. In addition, PT extract significantly shifted the gut microbiota of mice. DSS treatment significantly increased the portion of harmful bacteria (i.e., Helicobacter, Mucipirillum, and Parasutterella) and decreased the butyrate producing bacteria (i.e., Acetatifactor, Alistipes, Oscillibacter, and Clostridium_XIVb). PT extract increased the abundance of genera Clostridium_XIVb and also enriched some of predicted metabolic activities such as glyoxylate cycle, ethylmalonyl-CoA pathway, nitrate reduction, creatinine degradation, and glycine betaine metabolism. These results suggest that PT extract may ameliorate the DSS-induced colitis inflammation through regulating the compositions and functions of gut microbiota in mice.

Red beetroots, rich in betanin, may act as prebiotics and impact gut microbiota. Because the human gut microbiota is unique to each person, the effectiveness of prebiotics varies with the enterotype. In this study, we hypothesized that the effects of red beetroot powder (RP) and betanin pigment (BP) would differ depending on the enterotype. Fecal samples from 30 subjects were analyzed and categorized into three enterotypes: Phocaeicola, Prevotella, and Bifidobacterium. Feces were collected from one representative subject from each enterotype cluster for fermentation. Results showed that RP and BP affected microbiota composition and short-chain fatty acid (SCFA) production differently across enterotypes. The Bifidobacterium cluster showed significantly reduced alpha diversity, with the direction of change in the gut microbiota composition being different from that of other subjects. Additionally, SCFAs significantly increased, with the highest increase in the Bifidobacterium cluster. In this cluster, metabolic pathways related to SCFAs (i.e., starch and sucrose metabolism and glycolysis/gluconeogenesis) were altered. Conversely, Prevotella-dominant feces exhibited fewer changes in SCFAs and a lower increase in Bifidobacterium abundance than the others. These findings highlight that RP and BP elicit enterotype-specific responses in the gut microbiota composition and SCFA production, emphasizing the importance of enterotypes in personalized nutrition.

Various metabolic diseases caused by a high‐fat diet (HFD) are closely related to gut microbiota dysbiosis and epithelial barrier dysfunction. Polycan, a type of β‐glucan, is effective in treating anti‐obesity and metabolic diseases caused by HFD. However, the effect of Polycan on dysbiosis and epithelial barrier damage is still unknown. In this study, the effects of Polycan on dysbiosis and intestinal barrier damage were investigated using HFD‐induced obese model mice. C57BL/6 mice were fed a HFD for 12 weeks and treated with two different doses of Polycan (250 and 500 mg/kg) orally administered during weeks 9 to 12. Polycan supplementation increased the expression of tight junction genes (zonula occludens‐1, occludin, and claudin‐3) and short‐chain fatty acid (SCFA) content while reducing toxic substances (phenol, p ‐cresol, and skatole). Most significantly, Polycan enriched SCFA‐producing bacteria (i.e., Phocaeicola , Bacteroides , Faecalibaculum , Oscillibacter , Lachnospiraceae, and Muribaculaceae), and decreased the Firmicutes/Bacteroidetes ratio and toxic substances‐producing bacteria (i.e., Olsenella , Clostridium XVIII, and Schaedlerella ). Furthermore, microbial functional capacity prediction of the gut microbiota revealed that Polycan enriched many SCFA‐related KEGG enzymes while toxic substance‐related KEGG enzymes were depleted. These findings indicated that Polycan has the potential to alleviate HFD‐induced intestinal barrier damage by modulating the function and composition of the gut microbiota.