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Ulcerative colitis (UC) is an idiopathic, long-term inflammatory disorder of the colon, characterized by a continuous remitting and relapsing course. The intestinal mucus barrier is the first line at the interface between the host and microbiota and acts to protect intestinal epithelial cells from invasion. Data from patients and animal studies have shown that an impaired mucus barrier is closely related to the severity of UC. Depletion of the mucus barrier is not just the strongest but is also the only independent risk factor predicting relapse in patients with UC. Peroxisome proliferator-activated receptor gamma (PPARγ), a nuclear transcription regulator, is involved in the regulation of inflammatory cytokine expression. It is also known to promote mucus secretion under pathological conditions to expel pathogenic bacteria or toxins. More important, PPARγ has been shown to affect host-microbiota interactions by modulating the energy metabolism of colonocytes and the oxygen availability of the intestinal microbiome. It is well known that gut microbiota homeostasis is essential for butyrate generation by the commensal bacteria to supply energy resources for colonocytes. Therefore, it can be speculated that PPARγ, as a central coordinator of the mucus barrier, may be a promising target for the development of effective agents to combat UC.

Overconsumption of drinks containing fructose increases the risk for hyperuricemia and gout. Comparative analysis evaluating the indicators of serum uric acid (SUA) load caused by natural food-derived fructose and pure fructose in sweeteners is lacking. We aimed to uncover the effect of fructose from apple and honey and pure fructose powder on the SUA concentration of healthy young Chinese individuals.Two randomized crossover trials were performed. The participants were randomly assigned to consume apple or honey (test food) or pure fructose powder (reference food); one week later, the groups' dietary intervention was switched. Blood samples were collected at 0, 30, 60, and 120 min after meal to measure the SUA and blood glucose concentrations.At 30 and 60 min, the SUA concentration in participants consuming apple or honey was lower than in those consuming fructose powder. At 120 min, the SUA concentration of participants consuming apple returned to baseline. The areas under the curve (AUC) within 2 h (2h- AUCs) of SUA exhibited the trend of fructosehoneyapple. The 2h-AUC ratio between test food and reference food was determined using the uric acid index to assess the efficiency of food-derived fructose in increasing the SUA concentration. The uric acid index of honey was higher than that of apple. Men had higher postprandial SUA concentration than women.Food-derived fructose caused a lighter load on uric acid metabolism than pure fructose. Uric acid index can be useful for distinguishing fructose-containing foods.

The intestinal mucus barrier nourishes and tames the gut microbiota using its glycans during homeostasis. EPA fortifies the intestinal mucus barrier, this was mediated by coordination of the interaction between the host and gut microbiota.

To assess the causality of potentially modifiable factors, including lifestyle, nutrients, lipids, anthropometric traits, and inflammatory factors of Parkinson's disease (PD), genetic instruments for modifiable factors were identified from genome-wide association studies (GWAS).Genetic associations for PD (1,239 cases and 451,025 matched controls) were extracted from the UK Biobank GWAS summary statistics. The causal effects of modifiable factors on the risk of PD were estimated using the multiplicative random-effects inverse variance weighted method (IVW).In the IVW analysis, a decreased risk for PD was causally associated with genetically predicted smoking cessation (odds ratio 0.41, [95% confidence interval] 0.32-0.78; p0.001), and higher bone mineral density (0.43, 0.38 -0.71; p0.001), higher concentrations of vitamin B-12 (0.56, 0.43-0.91; p0.001), docosahexenoic acid (0.52, 0.37-0.71; p0.001), and sIL-6R (0.69, 0.58-0.75; p0.001). Instead, analysis further supported the role of apolipoprotein (a) isoform size(1.67, 1.36-1.71; p0.001), being a genetically morning person (2.18, 1.12-4.72; p0.001), and number of cigarette smoking (1.05, 1.01-1.08; p0.001) in contributing to the risk of developing PD.Our findings provide new evidence for the potential positive causal association of cigarette smoking number and apolipoprotein (a) isoform size and the inverse causal association of vitamin B-12, docosahexaenoic acid, smoking cessation, and soluble interleukin-6 receptor with PD, which contributes to the development of new interventions for PD.