Different Dose of Sucrose Consumption Divergently Influences Gut Microbiota and PPAR-γ/MAPK/NF-κB Pathway in DSS-Induced Colitis Mice

Abstract

Sugar reduction and sugar control are advocated and gaining popularity around the world. Sucrose, as the widely consumed ingredient in our daily diet, has been reported a relation to gastrointestinal diseases. However, the role of sucrose in inflammatory bowel disease remains controversial. Hence, our study aimed to elucidate the potential role of three doses of sucrose on DSS-induced colitis in C57BL/6 mice and the underlying mechanisms. The results showed that low-dose sucrose intervention alleviated colitis in mice, reducing the expression of inflammatory cytokines and repairing mucosal damages. In contrast, high-dose sucrose intervention exacerbated colitis. Furthermore, three doses of sucrose administration markedly altered gut microbiota composition. Notably, the low-dose sucrose restored microbial dysfunction and enhanced the production of short chain fatty acids (SCFAs). Specifically, the abundance of SCFAs-producing bacteria Faecalibaculum, Bacteroides, and Romboutsia were increased significantly in the LOW group. Consistently, PPAR-γ, activated by SCFAs, was elevated in the LOW group, thereby inhibiting the MAPK/NF-κB pathway. Together, our study demonstrates the differential effects of sucrose on colitis at different doses, providing a scientific basis for measuring and modifying the safe intake level of sugar and providing favorable evidence for implementing sugar reduction policies.

Microbiota alteration of Chinese young male adults with high-status negative cognitive processing bias

“…A correlation between SCFA levels and the abundance of Faecalibaculum, Romboutsia, Bacteroides, and Turicibacter were found in rats. Faecalibaculum was the most strongly positively correlated with the levels of SCFA levels, which are well known as the endogenous ligands of PPARγ, and crucially together with increasing PPARγ expression, promoting the PPARγ/MAPK/NF-κB signaling pathway connected with the metabolism and immune system (Zhang et al, 2022).…”

A screen of small molecule and genetic modulators of life span in female Drosophila identifies etomoxir, RH5849 and unanticipated temperature effects

“…The identification of mammalian PPARγ as a mifepristone target is of particular interest. PPARγ is a central regulator of lipid and glucose metabolism [ 9 ], and acts as an anti-inflammatory regulator in the gut [ 10 , 11 ], and as a regulator of lipid metabolism adaptation during pregnancy [ 12 ]. Thiazolidinedione drugs, including pioglitazone and rosiglitazone, have been used to treat diabetes based on their ability activate PPARγ [ 9 , 13 ].…”

Saffron Petal, an Edible Byproduct of Saffron, Alleviates Dextran Sulfate Sodium-Induced Colitis by Inhibiting Macrophage Activation and Regulating Gut Microbiota

“…Simultaneously, the compound−target network analysis indicated that astragalin, 2″-(6-acetylglucosyl)astragalin, sucrose, and narcissin were identified as the primary components responsible for the anti-inflammatory properties exhibited by SP extract. Previous studies have verified that both astragalin and low dose of sucrose could effectively alleviate the severity of colitis in mice 33,34 and also reported that astragalin and narcissin have potent anti-inflammatory effects against alveolar inflammation, osteoarthritis, and neuroinflammation by down-regulating MAPK and/or PI3K/Akt signaling pathways. 35−38 Taken together, these findings collectively indicate that SP extract possesses the ability to alleviate DSS-induced colonic 39 has been previously reported to reduce hepatocyte apoptosis and combat concanavin A-induced liver injury in a CD95dependent manner.…”