Elastic metal–organic materials (MOMs) capable of multiple stimuli‐responsiveness based on dual‐stress and thermally responsive triple‐helix coordination polymers are presented. The strong metal‐coordination linkage and the flexibility of organic linkers in these MOMs, rather than the 4 Å stacking interactions observed in organic crystals, causes the helical chain to act like a molecular spring and thus accounts for their macroscopic elasticity. The thermosalient effect of elastic MOMs is reported for the first time. Crystal structure analyses at different temperatures reveal that this thermoresponsiveness is achieved by adaptive regulation of the triple‐helix chains by fine‐tuning the opening angle of flexible V‐shaped organic linkers and rotation of its lateral conjugated groups to resist possible expansion, thus demonstrating the vital role of adaptive reorganization of triple‐helix metal–organic chains as a molecular spring‐like motif in crystal jumping.
The stability of many MOFs is not
satisfactory, which severely
limits the exploration of their potential applications. Given this,
we have proposed a strategy to improve the stability of MOFs by introducing
alkali metal K+ capable of coordinating with metal nodes,
which finally induces the interpenetrating uranyl-porphyrin framework
to connect as a whole (IHEP-9). The stability experiments
reveal that the IHEP-9 has good thermal stability up
to 400 °C and can maintain its crystalline state in the aqueous
solution with pH ranging from 2 to 11. The catalytic activity of IHEP-9 as a heterogeneous photocatalyst for CO2 cycloaddition under the driving of visible light at room temperature
is also demonstrated. This induced interpenetration and fixation method
may be promising for the fabrication of more functional MOFs with
improved structural stability.
Noncaloric artificial sweeteners (NAS) are extensively introduced into commonly consumed drinks and foods worldwide. However, data on the health effects of NAS consumption remain elusive. Saccharin and sucralose have been shown to pass through the human gastrointestinal tract without undergoing absorption and metabolism and directly encounter the gut microbiota community. Here, we aimed to identify a novel mechanism linking intestinal Akkermansia muciniphila and the aryl hydrocarbon receptor (AHR) to saccharin/sucralose-induced nonalcoholic fatty liver disease (NAFLD) in mice. Saccharin/sucralose consumption altered the gut microbial community structure, with significant depletion of A. muciniphila abundance in the cecal contents of mice, resulting in disruption of intestinal permeability and a high level of serum lipopolysaccharide, which likely contributed to systemic inflammation and caused NAFLD in mice. Saccharin/sucralose also markedly decreased microbiota-derived AHR ligands and colonic AHR expression, which are closely associated with many metabolic syndromes. Metformin or fructo-oligosaccharide supplementation significantly restored A. muciniphila and AHR ligands in sucralose-consuming mice, consequently ameliorating NAFLD.
IMPORTANCE Our findings indicate that the gut-liver signaling axis contributes to saccharin/sucralose consumption-induced NAFLD. Supplementation with metformin or fructo-oligosaccharide is a potential therapeutic strategy for NAFLD treatment. In addition, we also developed a new nutritional strategy by using a natural sweetener (neohesperidin dihydrochalcone [NHDC]) as a substitute for NAS and free sugars.
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