The systematic review and meta-analysis were conducted to ascertain the prevalence of anemia, iron deficiency (ID), and iron deficiency anemia (IDA) among Chinese pregnant women. A total of 722 articles on maternal anemia during pregnancy published between January 2010 and December 2020 were compiled, and a systematic review and meta-analysis were conducted on 57 eligible studies including 1,376,204 pregnant women to ascertain the prevalence of anemia and the prevalence in different subgroups. The results showed that the prevalence of anemia, ID, and IDA among pregnant women in China were 30.7% (95% CI: 26.6%, 34.7%), 45.6% (95% CI: 37.0%, 54.2%), and 17.3% (95% CI: 13.9%, 20.7%), respectively. All prevalence increased with the progression of the pregnancy. There were sizable regional variations in the prevalence of anemia, ID, and IDA. Generally, lower prevalence was observed in the economically more advanced eastern region of the country, while the prevalence of ID was higher in the eastern region than that in the western region. The prevalence of anemia and IDA in rural areas was higher than that in urban areas, but ID prevalence was higher in urban areas. In conclusion, the regional differences and urban–rural disparities in the prevalence of anemia indicate the need for more context-specific interventions to prevent and treat anemia. It was found that dietary factors were one of the major causes of anemia, and iron-containing supplements and nutrition counseling could be effective interventions to reduce the prevalence of anemia, ID, and IDA among Chinese pregnant women.

Obejectives: This study explored the immunomodulatory effects of a prebiotic formula consisting of 2′-fucosyllactose (2′-FL), galacto-oligosaccharides (GOSs), and fructo-oligosaccharides (FOSs) (hereinafter referred to as 2FGF) in cyclophosphamide (CTX)-induced immunosuppressed BALB/c mice and its underlying mechanisms. Methods: Sixty healthy female BALB/c mice were randomly divided into the following groups: normal control (NC) group; CTX treatment (CTX) group; 2FGF low-dose (2FGF-L) group; 2FGF medium-dose (2FGF-M) group; and 2FGF high-dose (2FGF-H) group. An immunosuppressed model was established in the 2FGF-H group by intraperitoneal injection of 80 mg/kg CTX. After 30 days of 2FGF intervention, peripheral blood, spleen tissue, thymus tissue, and intestinal tissue from the mice were collected and analyzed. The changes in weight and food intake of the mice were recorded weekly. Hematoxylin-eosin (HE) staining was used to observe the histological change of the spleen tissue. Enzyme-linked immunosorbent assay (ELISA) was employed to detect cytokine levels in peripheral blood. Flow cytometry was used to analyze T lymphocyte subgroup ratio of splenic lymphocytes. Western blot analysis was conducted on intestinal tissues to assess the expression of proteins involved in the tight junction, toll-like receptor 4 (TLR4), mitogen-activated protein kinase (MAPK), and nuclear factor kappa-light-chain-enhancer of activated B cell (NF-κB) signaling pathways. Additionally, molecular techniques were used to analyze the intestinal microbiota. Results: The results showed that 2FGF restored CTX-induced splenic injury, increased the number of splenic T lymphocytes, and elevated serum cytokines such as interleukin-4 (IL-4) and IL-10. In the intestine, 2FGF upregulated the expression of intestinal epithelial tight junction proteins such as Claudin-1 and zonula occludens 1 (ZO-1), thereby enhancing intestinal barrier function and activating the MAPK and NF-κB pathways via TLR4. Furthermore, 2FGF elevated the α-diversity (Shannon and Simpson indices) of the gut microbiota in CTX-induced immunosuppressed mice, enriching bacteria species positively correlated with anti-inflammatory cytokines (e.g., IL-4) such as g_Streptomyces and g_Bacillus and negatively correlated with pro-inflammatory cytokines (e.g., IL-1β) such as g_Saccharomyces. The results suggest that 2FGF may enhance immunity via the gut–immune axis. Conclusions: The 2FGF prebiotic formula showed an immunomodulatory effect in CTX-induced immunosuppressed mice, and the mechanism of which might involve optimizing the gut flora, enhancing intestinal homeostasis, strengthening the intestinal barrier, and promoting the expression of immune factors by regulating the TLR-4/MAPK/NF-κB pathway.

Objective: To investigate the effect of milk minerals on bone mineral density (BMD) and bone quality in growing rats and explore the underlying mechanisms related to calcium absorption, bone metabolism, and the gut–bone axis. Methods: Sixty healthy 4-week-old male Sprague-Dawley (SD) rats were randomly divided to five groups based on their body weight: Low-Calcium Control Group (Control), Low-Dose milk mineral Group (Low), Medium-Dose milk mineral Group (Medium), High-Dose milk mineral Group (High) and Calcium Carbonate Control Group (CaCO₃), which received the same dose level (elemental calcium) as the High group. The milk mineral dosage was set at 5, 10, and 15 times the human recommended intake of elemental calcium. After 12 weeks of intervention, femurs were collected for analysis of BMD, bone microstructure, and bone mechanical strength. Additionally, analyses included calcium levels in the femur, feces, and diet; serum bone metabolism biomarkers; tissue protein expression; as well as gut microbiota composition and short-chain fatty acid content. Result: Milk mineral exhibited non-inferior efficacy to CaCO₃ in increasing femoral calcium content, enhancing BMD, and improving bone microarchitecture. Notably, the Medium group achieved comparable bone-protective effects to the CaCO₃ group despite a 20.8% lower calcium content, which was accompanied by a relatively high calcium absorption rate (90.9% vs. 86.5%). With respect to serum markers, milk mineral maintained bone formation while suppressing bone resorption, resulting in a net anabolic state comparable to that of CaCO₃. Milk mineral significantly upregulated the protein expression of renal CYP27B1 and intestinal calcium ion transporters, and increased serum IGF-I levels. Furthermore, milk mineral promoted the enrichment of certain specific gut microbial genera, which showed a significant positive correlation with IGF-I, bone calcium content and BMD. Conclusions: Milk mineral supplementation appears to promote bone formation and mineralization in growing rats, accompanied by enhanced intestinal calcium absorption, enrichment of characteristic gut microbes and elevated microbial metabolite concentrations.