Gout is a metabolic disease and is the most common form of inflammatory arthritis affecting men. However, the pathogenesis of gout is still uncertain, and novel biomarkers are needed for early prediction and diagnosis of gout. The aim of this study was to develop a systemic metabolic profile of patients with asymptomatic hyperuricemia (HUA) and gout by using a metabolomics approach, and find potential pathophysiological mechanisms of and markers of predisposition to gout. Serum samples were collected from 149 subjects, including 50 patients with HUA, 49 patients with gout and 50 healthy controls. 1H nuclear magnetic resonance (NMR) spectroscopy combined with principal components analysis and orthogonal partial least squares-discriminant analysis were used to distinguish between samples from patients and healthy controls. Clinical measurements and pathway analysis were also performed to contribute to understanding of the metabolic change. By serum metabolic profiling, 21 metabolites including lipids and amino acids were significantly altered in patients with HUA or gout. The levels of identified biomarkers together with clinical data showed apparent alteration trends in patients with HUA or gout compared to healthy individuals. According to pathway analysis, three and five metabolic pathways were remarkably perturbed in patients with HUA or gout, respectively. These enriched pathways involve in lipid metabolism, carbohydrate metabolism, amino acids metabolism and energy metabolism. Taken together, we identified the biomarker signature for HUA and gout, which provides biochemical insights into the metabolic alteration, and identified a continuous progressive axis of development from HUA to gout.

Nonalcoholic steatohepatitis (NASH) is a subtype of nonalcoholic fatty liver disease (NAFLD). Either Lycium barbarum polysaccharide (LBP) or aerobic exercise (AE) has been reported to be beneficial to hepatic lipid metabolism. However, whether the combination of LBP with AE improves lipid accumulation of NASH remains unknown. Our study investigated the influence of 10 weeks of treatment of LBP, AE, and the combination (LBP plus AE) on high-fat-induced NASH in Sprague–Dawley rats. The results showed that LBP or AE reduced the severity of the NASH. LBP plus AE treatment more effectively ameliorated liver damage and lowered levels of serum lipid and inflammation. In addition, the combination can also regulate genes involved in hepatic fatty acid synthesis and oxidation. LBP plus AE activated AMPK, thereby increasing the expression of PPARα which controls hepatic fatty acid oxidation and its coactivator PGC-1α. Our study demonstrated the improvement of LBP plus AE on NASH via enhancing fatty acid oxidation (FAO) which was dependent on AMPK/PPARα/PGC-1α pathway.

The relationships between fine particulate matter (PM2.5) exposure and health effects are complex and incompletely understood. Evidence suggests that PM2.5 exposure alters gut microbiota composition and metabolites, but the connections between these changes remain unclear. The aim of our study was to investigate how gut microbiota are involved in the systemic metabolic changes following PM2.5 gastrointestinal exposure. We used multi-omics approaches, including 16S rRNA sequencing and serum metabolomics, to identify alterations in gut microbes and metabolites of PM2.5-exposed rats. We then explored correlations between perturbed gut microbiota and metabolic changes, and conducted pathway analyses to determine critical metabolic pathways impacted by PM2.5 exposure. To verify links between gut microbiome and metabolome disruptions, we performed fecal microbiota transplantation (FMT) experiment. A total of 30 differential gut microbe taxa were identified between PM2.5 and control groups, primarily in Firmicutes, Acidobacteria, and Proteobacteria phyla. We also identified 30 differential metabolites, including glycerophospholipids, fatty acyls, amino acids and others. Pathway analysis revealed disruptions in glycerophospholipid metabolism, steroid hormone biosynthesis, and linoleic acid metabolism. Through FMT, we confirmed PM2.5 altered phosphatidylcholine and linoleic acid metabolism by changing specific gut bacteria. Our results suggest that PM2.5 gastrointestinal exposure triggers systemic metabolic changes by disrupting the gut microbiome, especially glycerophospholipid and linoleic acid metabolism pathways.

This study aimed to gather the best evidence on the relationship between dietary factors and hyperuricaemia and gout. We searched databases including PubMed, Embase, Cochrane, and Web of Science from database creation to July 2023. Meta-analysis showed that consumption of alcohol (OR: 1.41, 95% CI: 1.29-1.55; 1.60, 95% CI: 1.33-1.93, respectively), red meat (OR:1.27, 95% CI: 1.18-1.37; 1.32, 95% CI: 1.18-1.47, respectively), fructose (OR: 1.29, 95% CI: 1.21-1.38; 1.65, 95% CI: 1.36-2.01, respectively) and seafoods (OR: 1.40, 95% CI: 1.20-1.64; 1.29, 95% CI: 1.00-1.67, respectively) were positively associated with the risk of hyperuricaemia and gout, while vegetables (OR: 0.78, 95% CI: 0.71-0.85; 0.96,95% CI 0.74-1.24, respectively) were inversely associated. Dairy products (OR: 0.69, 95% CI: 0.61-0.78) and nuts (OR: 0.75, 95% CI: 0.60-0.93) were also inversely associated with the risk of hyperuricaemia. Soy products (OR: 0.86, 95% CI: 0.75-0.98) and coffee (OR: 0.56, 95% CI: 0.39-0.81) were negatively associated with the risk of gout.

Lycium barbarum polysaccharides (LBPs) have been shown to exert an antiglycemic effect. Emerging evidence suggests that patients with hyperglycemia have a hypercontractility of duodenum, and targeting duodenal contraction of duodenum can be beneficial to glucose metabolism. However, it is unknown whether LBPs can improve glucose metabolism by regulating the hypercontractility of the duodenum. Our aim was to explore the effect of LBPs on duodenal contraction in prediabetic mice and also preliminarily investigate the mechanism. The results showed that LBPs improved glucose homeostasis by decreasing the duodenal amplitude of contraction rather than frequency. Moreover, LBPs ameliorated the gut microbiota composition and the levels of short-chain fatty acids, especially acetic acid, which might bind to the receptor on neurons to regulate the contraction of the duodenum. Acetic acid was hypothesized to play a key role in the above process. Then, acetic acid was determined to exert an antiglycemic effect as expected. In conclusion, LBPs may rely on acetic acid to regulate duodenal contraction to ameliorate glucose metabolism in prediabetic mice, which provides a new therapeutic strategy to treat dysglycemia.

Objective: Metabolic syndrome (MetS) represents a growing and significant public health burden worldwide. The evidence regarding whether skipping breakfast affects the development of MetS and its components remains inconsistent and uncertain. This study aimed to synthesize the best available evidence regarding the association between skipping breakfast and the risk of MetS and its components. Methods: This systematic review and meta-analysis was conducted in accordance with the PRISMA 2020 guidelines. We systematically searched the PubMed, Embase, Cochrane Library, and Web of Science databases from inception until May 2025. Two reviewers independently screened titles/abstracts and full texts, extracted data, and assessed the risk of bias. This review included cross-sectional and cohort studies on the association between breakfast skipping and the risk of MetS and its components. Results: Nine studies were included after quality evaluation by NOS. Pooled results from the meta-analysis revealed that skipping breakfast was significantly associated with an increased risk of MetS (OR: 1.10, 95% CI: 1.04–1.17) and its components—namely abdominal obesity (OR = 1.17, 95% CI 1.01–1.34), hypertension (OR: 1.21, 95% CI: 1.10–1.32), hyperlipidemia (OR: 1.13, 95% CI: 1.04–1.23), and hyperglycemia (OR = 1.26, 95% CI: 1.16–1.37). Conclusions: The meta-analysis demonstrated that skipping breakfast was significantly associated with an increased risk of MetS and its key components—abdominal obesity, hypertension, hyperlipidemia, and hyperglycemia. These findings highlight regular breakfast consumption as a potential modifiable factor for preventing and managing MetS and related cardiometabolic diseases.