Research has indicated that treatment with rosuvastatin can improve liver pathology in metabolic-associated fatty liver disease (MAFLD) patients and that treatment with Bifidobacterium can improve MAFLD. Therefore, the effects of Bifidobacterium, rosuvastatin, and their combination on related indices in a rat model of diet-induced MAFLD need to be investigated. Forty rats were divided into five groups: the normal diet group (N), high-fat diet (HFD) model group (M), HFD + probiotic group (P), HFD + statin group (S), and HFD + probiotic + statin group (P-S). To establish the MAFLD model, the rats in Groups M, P, S, and P-S were fed a HFD for 8 weeks. The treatments included saline in Group N and either Bifidobacterium, rosuvastatin, or their combination in Groups P, S, and P-S by intragastrical gavage. After 4 weeks of intervention, the rats were euthanized, and samples were harvested to analyze gastrointestinal motility and liver function, pathological changes, inflammatory cytokine production, and the expression of proteins in key signaling pathways. HFD feeding significantly increased the body weight, liver index, and insulin resistance (IR) index of the rats, indicating that the MAFLD model was successfully induced. Bifidobacterium reduced the liver of MAFLD rats, while Bifidobacterium with Rosuvastatin decreased the liver index, IR index, and levels of aspartate aminotransferase and alanine aminotransferase in MAFLD rats. The MAFLD model showed altered expression of proteins in signaling pathways that regulate inflammation, increased production of inflammatory cytokines, an elevated MAFLD activity score (MAS), and pathological changes in the liver. The MAFLD model also showed reduced relative counts of intestinal neurons and enteric glial cells (EGCs), altered secretion of gastrointestinal hormones, and slowed gastrointestinal emptying. Bifidobacterium, rosuvastatin, or their combination inhibited these various changes. HFD feeding changed the rats’ gut microbiota, and the tested treatments inhibited these changes. These results suggest that the gastrointestinal motility disorder and abnormal liver function in MAFLD rats may be related to a reduction in Escherichia-Shigella bacteria and an increase in Asticcacaulis bacteria in the gut microbiota and that the improvement in liver function induced by Bifidobacterium plus rosuvastatin may be related to increases in Sphingomonas and Odoribacter bacteria and a decrease in Turicibacter bacteria in the gut microbiota. The combined use of Bifidobacterium and rosuvastatin could better regulate the gut microbiota of MAFLD model rats, promote gastrointestinal emptying, and improve liver pathology and function than single treatment with Bifidobacterium or rosuvastatin. This provides a better strategy for the treatment of MAFLD.

BACKGROUND A high-fat diet (HFD) can cause systemic low-grade inflammation, metabolic and inflammatory diseases, and alter the composition of intestinal microbiota. Although probiotics mitigate intestinal inflammation, it is still unclear whether they can directly inhibit the production of deoxycholic acid (DCA) to prevent or alleviate intestinal inflammation. AIM To investigate changes in intestinal flora, fecal DCA levels, and cytokine profiles. METHODS Vancomycin was administered to significantly reduce the population of intestinal gram-positive bacteria, which helped in reducing the fecal DCA levels. Recruitment of pro-inflammatory macrophages, polarization of macrophages, and the inflammation associated with the intestinal flora of the HFD animal model were assessed. Their expression levels were analyzed through real-time polymerase chain reaction, immunofluorescence staining, liquid chromatography-mass spectrometry, and 16S rRNA high-throughput sequencing. RESULTS HFD or DCA promotes the infiltration of colon macrophages, causing their polarization toward the M1 phenotype. This polarization can be inhibited by both vancomycin and Bifidoba cterium . Bifidobacterium enhances the species richness and uniformity of the intestinal microbiota in HFD mice; however, it does not improve these parameters in the presence of vancomycin. Bifidobacterium also does not increase the abundance of microbiota in HFD-fed or HFD-and-vancomycin-treated mice. HFD alters the relative abundance of intestinal microbiota at the phylum and genus levels. Bifidobacterium or vancomycin can partially mitigate these changes. CONCLUSION Bifidobacterium can inhibit HFD-induced intestinal inflammation or that resulting from DCA-induced M1 polarization of macrophages. It may also regulate bile acid levels and target cholesterol metabolism pathways, which may serve as potential therapeutic strategies for HFD-associated colitis.

Small intestinal bacterial overgrowth (SIBO) has recently garnered significant attention from both medical professionals and the general public, likely due to its increasing prevalence and advancements in testing technology. However, the accuracy of breath tests in clinical practice for diagnosing SIBO still requires thorough validation. This review compiles the definition, etiology, influencing factors, novel testing methods, and the determination and interpretation of SIBO results. We particularly discuss the various controversies and limitations associated with these tests. By comparing and evaluating the advantages and disadvantages of different diagnostic methods fo rSIBO, we aim to enhance the understanding of its clinical diagnosis and promote future research focused on accurate detection methods.