This study was aimed at determining potential effects of apple-derived pectin on weight gain, gut microbiota, gut barrier and metabolic endotoxemia in rat models of diet-induced obesity. The rats received a standard diet (control; Chow group; n = 8) or a high-fat diet (HFD; n = 32) for eight weeks to induce obesity. The top 50th percentile of weight-gainers were selected as diet induced obese rats. Thereafter, the Chow group continued on chow, and the diet induced obese rats were randomly divided into two groups and received HFD (HF group; n = 8) or pectin-supplemented HFD (HF-P group; n = 8) for six weeks. Compared to the HF group, the HF-P group showed attenuated weight gain (207.38 ± 7.96 g vs. 283.63 ± 10.17 g, p < 0.01) and serum total cholesterol level (1.46 ± 0.13 mmol/L vs. 2.06 ± 0.26 mmol/L, p < 0.01). Compared to the Chow group, the HF group showed a decrease in Bacteroidetes phylum and an increase in Firmicutes phylum, as well as subordinate categories (p < 0.01). These changes were restored to the normal levels in the HF-P group. Furthermore, compared to the HF group, the HF-P group displayed improved intestinal alkaline phosphatase (0.57 ± 0.20 vs. 0.30 ± 0.19, p < 0.05) and claudin 1 (0.76 ± 0.14 vs. 0.55 ± 0.18, p < 0.05) expression, and decreased Toll-like receptor 4 expression in ileal tissue (0.76 ± 0.58 vs. 2.04 ± 0.89, p < 0.01). The HF-P group also showed decreased inflammation (TNFα: 316.13 ± 7.62 EU/mL vs. 355.59 ± 8.10 EU/mL, p < 0.01; IL-6: 51.78 ± 2.35 EU/mL vs. 58.98 ± 2.59 EU/mL, p < 0.01) and metabolic endotoxemia (2.83 ± 0.42 EU/mL vs. 0.68 ± 0.14 EU/mL, p < 0.01). These results suggest that apple-derived pectin could modulate gut microbiota, attenuate metabolic endotoxemia and inflammation, and consequently suppress weight gain and fat accumulation in diet induced obese rats.

The estimated prevalence of malnutrition in patients after major abdominal surgery ranges from 20% to 70%^1,2 and is associated with increased morbidity, such as impaired wound healing, hospital-acquired infection, postoperative complications, prolonged hospital stay, and increased mortality.^3-5 It is well documented that the catabolic response to surgery causes the depletion of essential nutrients, resulting in an increased risk of postoperative complications, particularly infectious complications. Therefore, timely and adequate energy supply is essential for maintaining optimal cell and organ function, promoting wound repair, and decreasing infectious complications after surgery.

Lack of enteral nutrition (EN) during parenteral nutrition (PN) leads to higher incidence of infection because of gut barrier dysfunction. However, the effects of partial EN on intestina linnate immunity, intestinal alkaline phosphatase (IAP) and microbiota remain unclear. The mice were randomized into six groups to receive either standard chow or isocaloric and isonitrogenous nutritional support with variable partial EN to PN ratios. Five days later, the mice were sacrificed and tissue samples were collected. Bacterial translocation, the levels of lysozyme, mucin 2 (MUC2), and IAP were analyzed. The composition of intestinal microbiota was analyzed by 16S rRNA pyrosequencing. Compared with chow, total parenteral nutrition (TPN) resulted in a dysfunctional mucosal barrier, as evidenced by increased bacterial translocation (p < 0.05), loss of lysozyme, MUC2, and IAP, and changes in the gut microbiota (p < 0.001). Administration of 20% EN supplemented with PN significantly increased the concentrations of lysozyme, MUC2, IAP, and the mRNA levels of lysozyme and MUC2 (p < 0.001). The percentages of Bacteroidetes and Tenericutes were significantly lower in the 20% EN group than in the TPN group (p < 0.001). These changes were accompanied by maintained barrier function in bacterial culture (p < 0.05). Supplementation of PN with 20% EN preserves gut barrier function, by way of maintaining innate immunity, IAP and intestinal microbiota.

Oral microecological agents show potential in reshaping intestinal microbiota and treating inflammatory bowel disease (IBD), but their clinical application is hindered by gastrointestinal challenges, antioxidant instability, and ineffective targeted delivery. In this study, we proposed a protective modification strategy utilizing a nanozyme coating and an alginate microsphere system to enhance the delivery efficiency, effectiveness, and precision of probiotics. By incorporating Mn into CeO₂, Mn@CeO₂ nanozyme was synthesized, significantly boosting ROS scavenging activity both in vitro and in vivo at safe dosages. Following the coincubation of Mn@CeO₂ with Limosilactobacillus reuteri, the nanozymes were successfully distributed onto the surface of the probiotics. MnCe@LR/AMs were then fabricated using the electrostatic spray method, enhancing their tolerance to the acidic environment of the stomach. Notably, sodium alginate (SA), through electrostatic interactions and binding to mannose receptors highly expressed at inflamed sites, conferred a dual-targeting property to MnCe@LR/AMs. In the treatment of colitis in mice, MnCe@LR/AMs were shown to function through the synergistic antioxidant and anti-inflammatory activities of their components. They also effectively reinforced the intestinal barrier, while improving gut microbial diversity and increasing the relative abundance of probiotics. Furthermore, we demonstrated that MnCe@LR/AMs contribute to the maintenance of intestinal homeostasis by enhancing the absorption of amino acids in the gut and modulating macrophage polarization to regulate the immune response. These findings suggest that MnCe@LR/AMs hold significant promise for developing advanced IBD therapies, offering improved precision and efficacy in probiotic delivery.

Background: Malnutrition is a common and critical problem that influences outcome in cancer patients. Body composition reflects a patient’s metabolic profile and physiologic reserves, which might be the true determinant of prognosis. In the present study, which aimed to identify valuable new prognostic indicators, we investigated the association between computed tomography–quantified body composition and short-term outcomes after gastrectomy for gastric cancer. Methods: Skeletal muscle index, mean muscle attenuation, and ratio of visceral-to-subcutaneous adipose tissue area (VSR) were calculated from preoperative computed tomography images. Low skeletal muscle index, low mean muscle attenuation, and high VSR were respectively termed “sarcopenia,” “myosteatosis,” and “visceral obesity.” The association of body composition with postoperative complications and serum markers of nutrition and inflammation after radical gastrectomy were analyzed. Results: The overall complication rate was significantly higher in the sarcopenia (62.5% vs. 27.3%, p = 0.001) and myosteatosis groups (38.2% vs. 4%, p = 0.002). Patients with visceral obesity had a higher incidence of inflammatory complications (20.3% vs. 6.5%, p = 0.01). Multivariate logistic regression analysis demonstrated that sarcopenia (p = 0.013), myosteatosis (p = 0.017), and low serum retinol-binding protein (p = 0.019) were independent risk factors for overall complications. Compared with control subjects, patients with sarcopenia had lower postoperative levels of serum retinol-binding protein (p = 0.007), and patients with visceral obesity had higher levels of C-reactive protein (p = 0.026). Conclusions: Sarcopenia, myosteatosis, and visceral obesity were significantly associated with increased rates of postoperative complications and affected the postoperative nutrition and inflammation status of patients with gastric cancer.