Type 3 resistant starch from Canna edulis modulates obesity and obesity-related low-grade systemic inflammation in mice by regulating gut microbiota composition and metabolism.

Obesity is a most prevalent human health problem. Several studies showed that appropriate modulation of gut microbiota could help reshape the metabolic profile of obese individuals, thereby altering the development of obesity. A nutritional strategy for treating obesity includes prebiotics. Type 3 Resistant Starch from Canna edulis (Ce-RS3) is a dietary fiber that exerts potential effects on the intestinal microbial community; however, the metabolic landscape and anti-obesity mechanism remain unclear. In the present study, obese mice were treated with Ce-RS3, and 16S rRNA gene sequencing and metabolomics were used to measure changes in gut microbiota and fecal metabolic profiles, respectively. At the end of the treatment (13 weeks), we observed slow weight gain in the mice, and pathological damage and inflammation were substantially reduced. Ce-RS3 constructs a healthy gut microbiota structure and can enhance intestinal immunity and reduce metabolic inflammation. Ce-RS3 increased the diversity of gut microbiota with enrichment of Bifidobacterium and Roseburia. Ce-RS3 regulated the systemic metabolic dysbiosis in obese mice and adjusted 26 abnormal metabolites in amino acids and lipids metabolism, many of which are related to the microbiome. More importantly, we found that the anti-obesity effect of Ce-RS3 can be transferred by fecal transplantation. The beneficial effects of Ce-RS3 might derive from gut microbiota changes, which might improve obesity and metabolic inflammation by altering host-microbiota interactions with impacts on the metabolome. In conclusion, Ce-RS3 can be used as a prebiotic with potential value for the treatment of obesity.

Preparation, structure characterization, and specific gut microbiota properties related to anti-hyperlipidemic action of type 3 resistant starch from Canna edulis.

Type 3 resistant starch (RS3) was developed from Canna edulis (Ce) native starch (NS) through dual enzymatic hydrolysis and recrystallization. Thereafter, the processed Ce-RS3 was subjected to systematic characterizations for its structural properties, anti-hyperlipidemic effect, and in vivo gut microbiota modulatory function. The Ce-RS3 content was increased to 49.11% after processing under optimal conditions. Compared with NS, Ce-RS3 maintained its B-type crystallization without introducing new chemical groups. Meanwhile, it displayed coarse surfaces, higher crystallinity, more ordered structures, and a higher proportion of chains with degree of polymerization (DP) 37-100. Ce-RS3 intervention significantly alleviated dyslipidemia in hyperlipidemic mice, which was associated with increased gut microbial diversity and unique microbial enrichment, potentially mediated by its fine structure. These observations are valuable for developing RS3 from C. edulis for prebiotics applications and support the potential strategy that utilizes well-designed RS to modulate specific bacterial populations to improve health.

Mechanisms of bergenin treatment on chronic bronchitis analyzed by liquid chromatography-tandem mass spectrometry based on metabolomics.

With increasing air pollution, chronic bronchitis (CB) has become a major public health problem worldwide. Previous studies have shown beneficial effects of Bergenin (Ber) on chronic bronchitis. To facilitate understanding of the pathogenesis underlying CB as well as to elucidate the Ber therapeutic mechanism, it is crucial to confirm the rational biomarkers of CB and its treatment. This study aimed to investigate the preventive chronic bronchitis mechanism of Ber by applying a serum metabolomics strategy. In this study, 18 Sprague-Dawley rats were randomly divided into three groups,with six rats in each group. Rats from the CB and Ber groups were exposed to tobacco smoke for 1 hd-1 (1 h per day) for 28 days. Ber was administered orally to Ber rats 3 h after exposure every day, and the others were administered water. According to the morphometric analysis of the airway epithelium and the count of white blood cells in the bronchoalveolar lavage fluid, Ber suppressed the infiltration of inflammatory cells, inhibited the secretion of mucus, and reduced white blood cells in bronchoalveolar lavage fluid. The metabolic profiles of sera were analyzed by multivariate statistical analyses, including PCA, PLS-DA and OPLS-DA models, and revealed that the levels of thirteen metabolites were significantly changed and identified as potential biomarkers in the CB group and Ber group. The results suggested that the therapeutic mechanism of Ber may be related to the regulation of dysfunctions in glycerophospholipid, tryptophan, arginine and proline metabolism induced by CB, and changes in arachidonic acid metabolism.

Tandem mass tags labeled quantitative proteomics to study the effect of tobacco smoke exposure on the rat lung.

BACKGROUND: The causal link between tobacco smoke exposure (TSE) and numerous severe respiratory system diseases (RSD), including chronic bronchitis, chronic obstructive pulmonary disease, and lung cancer, is well established. However, the pathogenesis of TSE-induced RSD remains incompletely understood. This research aims to detect the pathogenetic mechanisms and potential therapeutic targets of TSE-induced RSD. METHODS: This study employed TSE model which rats were exposed to a concentration of 60% tobacco smoke in a toxicant exposure system for four weeks. Tandem mass tags (TMT) labeled quantitative proteomics combined with off-line high pH reversed-phase fractionation, and nano-liquid chromatography-mass spectrometry method (off-line high pH RPF-nano-LC-MS/MS) were adopted to detect differentially expressed proteins (DEPs) in the lung tissues of the TSE model rats and to compare them with those in control. The accuracy of the results was verified by western blot. RESULTS: Compared with the control group, 33 proteins in the TSE model group's lung tissues showed significant differential expression. Analysis based on the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways indicated that, several biological pathways, such as the steroid biosynthesis pathway, were involved and played significant roles in the pathogenesis of the experimental group's TSE. CONCLUSIONS: These findings make a crucial contribution to the search for a comprehensive understanding of TSE-induced RSD's pathogenesis, and furthermore provide guidance for the diagnosis and treatment of TSE-induced RSD.