Obesity is a metabolic syndrome worldwide that causes many chronic diseases. Recently, we found an antiobesity effect of flaxseed polysaccharide (FP), but the mechanism remains to be elucidated. In this study, rats were first induced to develop obesity by being fed a high-fat diet. The obese rats were then fed a control diet, AIN-93M (group HFD), or a 10% FP diet (group FPD). The body weight, body fat, adipose tissue and liver sections, serous total triglycerides, levels of fasting blood glucose in serum, serous insulin, inflammatory cytokines in serum, and serous proteins within the leptin−neuropeptide Y (NPY) and AMP-activated protein kinase (AMPK) signaling pathway were determined and analyzed. FP intervention significantly reduced body weight and abdominal fat from 530 ± 16 g and 2.15% ± 0.30% in group HFD to 478 ± 10 g and 1.38% ± 0.48% in group FPD, respectively. This effect was achieved by removing leptin resistance possibly by inhibiting inflammation and recovering satiety through the significant downregulation of NPY and the upregulation of glucagon-like peptide 1. Adiponectin was then significantly upregulated probably via the gut−brain axis and further activated the AMPK signaling pathway to improve lipid metabolism including the improvement of lipolysis and fatty acid oxidation and the suppression of lipogenesis. This is the first report of the proposed antiobesity mechanism of FP, thereby providing a comprehensive understanding of nonstarch polysaccharides and obesity.

The current dietary recommendations for disease prevention and management are scarce and are not well supported. Beta‐glucan or quercetin in a diet can alleviate colorectal cancer (CRC) by regulating the gut microbiota and related genes, but the effects of alternating their consumption for routine ingestion during CRC occurrence remain unknown. This study investigated the effects of alternating the consumption of β‐glucan and quercetin for routine ingestion on CRC development in mice. The mortality rate, colonic length, inflammatory cytokines, gut microbiota, and colonic epithelial gene expression in healthy and CRC mice that consumed normal and alternate diets were compared and studied. The results showed that alternating the consumption of β‐glucan and quercetin (alternating among a β‐glucan diet, a normal diet and a normal diet that was supplemented with quercetin) alleviated colon damage and reduced the mortality rate in CRC mice, with a reduction in mortality of 12.5%. Alternating the consumption of β‐glucan and quercetin significantly decreased the TNF‐α level, increased the relative abundance of Parabacteroides, and downregulated three genes (Hmgcs2, Fabp2, and Gpt) that are associated with inflammation and cancer. Alternating the consumption of some bioactive compounds, such as β‐glucan and quercetin, in food can contribute to human health. This experiment provided some experimental evidence for the dietary recommendations for disease prevention and management.

Mucin 2 (MUC2) is the skeleton of colonic mucus that comprises the physical intestinal barrier. Different dietary polysaccharides may affect colonic mucus at different extents. The effect of pectin on MUC2 production is contradictory. To investigate whether and how pectin affected hosts’ colonic mucus, the amount of MUC2 in colon, the cecal, mucosal microbiota, and metabolites profiles were analyzed and compared with inulin. The results showed pectin stimulated the production of MUC2 at a similar level to inulin. Both interventions increased the abundance of cecal Lachnospira and Christensenellaceae_R‐7_group, and enhanced the production of specific metabolites including soyasapogenol B 24‐O‐b‐d‐glucoside, lucyoside Q, trans‐EKODE‐(E)‐Ib, and 1,26‐dicaffeoylhexacosanediol. Additionally, pectin increased the relative abundance (RA) of cecal Lactobacillus, and induced less RA of potentially harmful bacteria such as Helicobacter in mucosal microbiota than inulin. In conclusion, we first reported that pectin and inulin stimulated the mucus formation at a similar level. Two genera of cecal bacteria and four metabolites may play an important role in enhancing the production of MUC2. Moreover, the MUC2 production may be unrelated to several traditional health‐beneficial bacteria; pectin possibly performed as good as or better than the inulin in rats’ gut.

BackgroundObesity is one of the most serious public health challenges. Recently, we found that flaxseed polysaccharide (FP) had an anti-obesity effect through promoting lipid metabolism, inducing satiety and regulating gut microbiota, but how FP promote lipid metabolism through altering the colonic epithelial cells remains to be elucidated. In this study, a transcriptome study was performed to investigate the effect of FP altering the gene expression of colonic epithelial cells in an obese rat model. ResultsThe transcriptome analysis showed that 3,785 genes were differentially expressed after FP intervention in colonic epithelial cells, including 374 down-regulated and 3,411 up-regulated genes. Through KEGG analysis, we found out three classical pathways related to lipid metabolism and energy metabolism, including PPAR signaling pathway, nitrogen metabolism and oxidative phosphorylation (OXPHOS). Moreover, qRT-PCR results showed consistent expression trends of differential genes with transcriptome analysis. ConclusionsThe anti-obesity effect of FP may be achieved by regulating the expression of lipid metabolism- and energy metabolism-related proteins acting on the PPAR (peroxisome proliferator-activated receptor) signaling pathway, nitrogen metabolism and OXPHOS pathway in vivo.