High-fructose diet induced changes in gut microbiota structure and function, which have been linked to inflammatory response. However, the effect of small or appropriate doses of fructose on gut microbiota and inflammatory cytokines is not fully understood. Hence, the abundance changes of gut microbiota in fructose-treated Sprague-Dawley rats were analyzed by 16S rRNA sequencing. The effects of fructose diet on metabolic disorders were evaluated by blood biochemical parameter test, histological analysis, short-chain fatty acid (SCFA) analysis, ELISA analysis, and Western blot. Rats were intragastrically administered with pure fructose at the dose of 0 (Con), 2.6 (Fru-L), 5.3 (Fru-M), and 10.5 g/kg/day (Fru-H) for 20 weeks. The results showed that there were 36.5% increase of uric acid level in the Fru-H group when compared with the Con group. The serum proinflammatory cytokines (IL-6, TNF-α, and MIP-2) were significantly increased ( ), and the anti-inflammatory cytokine IL-10 was significantly decreased ( ) with fructose treatment. A higher fructose intake induced lipid accumulation in the liver and inflammatory cell infiltration in the pancreas and colon and increased the abundances of Lachnospira, Parasutterella, Marvinbryantia, and Blantia in colonic contents. Fructose intake increased the expressions of lipid accumulation proteins including perilipin-1, ADRP, and Tip-47 in the colon. Moreover, the higher level intake of fructose impaired intestinal barrier function due to the decrease of the expression of tight junction proteins (ZO-1 and occludin). In summary, there were no negative effects on body weight, fasting blood glucose, gut microbiota, and SCFAs in colonic contents of rats when fructose intake is in small or appropriate doses. High intake of fructose can increase uric acid, proinflammatory cytokines, intestinal permeability, and lipid accumulation in the liver and induce inflammatory response in the pancreas and colon.

Coarse cereals rich in polyphenols, dietary fiber, and other functional components exert multiple health benefits. We investigated the effects of cooked oats, tartary buckwheat, and foxtail millet on lipid profile, oxido-inflammatory responses, gut microbiota, and colonic short-chain fatty acids composition in high-fat diet (HFD) fed rats. Rats were fed with a basal diet, HFD, oats diet (22% oat in HFD), tartary buckwheat diet (22% tartary buckwheat in HFD), and foxtail millet diet (22% foxtail millet in HFD) for 12 weeks. Results demonstrated that oats and tartary buckwheat attenuated oxidative stress and inflammatory responses in serum, and significantly increased the relative abundance of Lactobacillus and Romboutsia in colonic digesta. Spearman’s correlation analysis revealed that the changed bacteria were strongly correlated with oxidative stress and inflammation-related parameters. The concentration of the butyrate level was elevated by 2.16-fold after oats supplementation. In addition, oats and tartary buckwheat significantly downregulated the expression of sterol regulatory element-binding protein 2 and peroxisome proliferator-activated receptors γ in liver tissue. In summary, our results suggested that oats and tartary buckwheat could modulate gut microbiota composition, improve lipid metabolism, and decrease oxidative stress and inflammatory responses in HFD fed rats. The present work could provide scientific evidence for developing coarse cereals-based functional food for preventing hyperlipidemia.

The dysbiosis of intestinal microbiota and their metabolites is linked to the occurrence and development of metabolic syndrome. Although fructose has been proven to be associated with worsened mucus in the colon, its mechanism remains unclear. In this study, we evaluated the relatively low intake of sucrose and fructose in the experimental colitis of Sprague Dawley rats by investigating the microbiome and metabolome. Results showed that sucrose and fructose significantly reduced body weight, colon length and increased inflammation infiltration in colon. Sucrose and fructose worsen colon functions by inhibiting the expression of tight junction (TJ) protein ZO-1 and increasing the level of lipopolysaccharide neoandrographolide (LPS) in plasma, while fructose was more significant. Furthermore, sucrose and fructose significantly changed the composition of gut microbiota characterized by decreasing Adlercreutzia, Leuconostoc, Lactococcus and Oscillospira and increasing Allobaculum and Holdemania along with reducing histidine, phenylalanine, arginine, glycine, aspartic acid, serine, methionine valine, alanine, lysine, isoleucine, leucine, threonine, tryptophan, tyrosine, proline, citrulline, 4-hydroxyproline and gamma amino butyric acid (GABA). Metabolome results showed that fructose may aggravate experimental colitis symptoms by inducing amino metabolism dysbiosis in the colon. These findings suggested that fructose worsened colitis by manipulating the crosstalk between gut microbiota and their metabolites.

In the exploration of the relationship between nutrition and health, dietary polyphenols, as bioactive substances derived from natural plants, have attracted much attention due to their diverse functional properties. Their health effects are highly dependent on the metabolic transformation by intestinal flora. The complex interaction between polyphenols and gut microbiota, as well as their role in the prevention and treatment of intestinal diseases, has become a research hotspot in the fields of nutrition and medicine. This review systematically explains the sources and classifications of polyphenols, points out their natural characteristic of low bioavailability. It also explores their intervention effects on intestinal diseases, analyzes the bidirectional action mechanism between polyphenols and gut microbiota, and elaborates on the specific pathways through which polyphenols improve intestinal diseases by regulating gut microbiota. Collectively, this review provides critical theoretical basis on polyphenols improving intestinal diseases for future research and clinical applications.

Background: A growing number of researches supported that dietary fructose was associated with most of the key features of metabolic syndrome (MetS). However, there was no related epidemiological studies among Chinese population, despite the sharp increase in MetS cases. This study explores the relationship between dietary fructose and MetS among Chinese residents aged 45 and above.Methods: A total of 25,528 participants (11,574 males and 13,954 females) were included in this nationwide representative cross-sectional study of China National Nutrition and Health Survey. Dietary fructose intake was assessed by 3-day 24-h dietary records. MetS was defined by the International Diabetes Federation and Chinese Diabetes Society criteria.Results: The consumption of dietary fructose was 11.6 g/day for urban residents and 7.6 g/day for rural residents. Fruits and vegetables as well as their products were the main sources of fructose intake. There was no association between dietary fructose intake and the odds of having MetS in both urban (P = 0.315) and rural residents (P = 0.230) after adjustment for confounding factors. Moreover, for urban residents participating physical activities, the odds of having MetS in the fourth quartiles (OR: 0.67; 95%CI: 0.52-0.87) was lower than that in the first quartile. In the sensitivity analysis, a significant reduction in the odds of having MetS was also found in the fourth quartiles (OR, 95%CI: 0.68, 0.51-0.90; 0.67, 0.49-0.91; 0.74, 0.56-0.99) compared with the first quartile when excluding smokers, alcohol users, and underweight/obesity, respectively. And there was no association between dietary fructose intake and the odds of having MetS after multivariate adjustment stratified by gender, smoking and alcohol use.Conclusions: Under the current dietary fructose intake status, there was no association between dietary fructose intake and the odds of having MetS among Chinese residents aged 45 and above. Physical activity and relatively low fructose intake may have a beneficial synergistic effect on MetS.