Dataset Information

Comprehensive Evaluation of Anti-hyperuricemic Effect of Red Kidney Bean Anthocyanins and Molecular Screening of the Lead Candidate

ABSTRACT:

Hyperuricemia (HUA) has emerged as an increasingly prevalent metabolic disorder worldwide. This study aimed to investigate the effects of red kidney bean (Phaseolus vulgaris L.) anthocyanins (RKBA) on alleviating HUA and screen the lead candidate. RKBA effectively inhibited XOD in vitro. In vivo results showed that RKBA significantly reduced serum uric acid levels (p < 0.05), protected kidney function, alleviated inflammation and tissue damage in vivo. Mechanistically, RKBA down-regulated xanthine oxidase, adenosine deaminase and 5′-nucleotidase while modulating urate transporters URAT1, GLUT9 and OAT3, thereby rebalancing uric-acid metabolism. Additionally, it reshaped the gut microbiome (particularly increasing Ligilactobacillus and Dubosiella), and elevated short-chain fatty acids. Subsequently, UPLC-ESI-MS/MS-based anthocyanin-targeted omics identified and quantified 42 anthocyanins, which is the most comprehensive RKBA profiling to date. Ultimately, integrating molecular docking and dynamics simulation, pelargonidin-3,5-diglucoside was selected as the lead candidate owing to its high abundance and strong affinity for xanthine oxidase, which was further confirmed by in vitro experiment. Pelargonidin-3,5-diglucoside has not been reported as an anti-hyperuricemic nutraceutical before, hence this study lays a foundation for future in vivo validation.

INSTRUMENT(S): Liquid Chromatography MS - alternating - reverse phase

PROVIDER: MTBLS13234 | MetaboLights | 2025-10-29

REPOSITORIES: MetaboLights

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Source:

			Action	DRS
	a_MTBLS13234_LC-MS_alternating_reverse-phase_metabolite_profiling.txt	Txt
	i_Investigation.txt	Txt
	m_MTBLS13234_LC-MS_alternating_reverse-phase_metabolite_profiling_v2_maf.tsv	Tabular
	s_MTBLS13234.txt	Txt

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Project description:Metabolic pathways are largely conserved in eukaryotes, but the transcriptional regulation of these pathways can sometimes vary between species; this has been termed rewiring. Recently it has been established that in the Saccharomyces lineage starting from Saccharomyces castelli, genes involved in allantoin breakdown have been genomically relocated to form the DAL cluster. The formation of the DAL cluster occurred along with the loss of urate permease (UAP) and urate oxidase (UOX), reducing the requirement for oxygen and bypassing the candidate Ppr1 inducer, uric acid. In Saccharomyces cerevisiae this allantoin catabolism cluster is regulated by the transcription factor Dal82, which is not present in many of the pre-rearrangement fungal species. We have used ChIP-Chip analysis, transcriptional profiling of an activated Ppr1 protein, bioinformatics, and nitrogen utilization studies, to establish that in Candida albicans the zinc cluster transcription factor Ppr1 controls this allantoin catabolism regulon. Intriguingly, in S. cerevisiae the Ppr1 ortholog binds the same DNA motif (CGG(N6)CCG) as in C. albicans, but serves as a regulator of pyrimidine biosynthesis. This transcription factor rewiring appears to have taken place at the same phylogenetic step as the formation of the rearranged DAL cluster. This transfer of the control of allantoin degradation from Ppr1 to Dal82, together with the repositioning of Ppr1 to the regulation of pyrimidine biosynthesis, may have resulted from a switch to a metabolism that could exploit hypoxic conditions in the lineage leading to S. castellii and S. cerevisiae. Metabolic pathways are largely conserved in eukaryotes, but the transcriptional regulation of these pathways can sometimes vary between species; this has been termed rewiring. Recently it has been established that in the Saccharomyces lineage starting from Saccharomyces castelli, genes involved in allantoin breakdown have been genomically relocated to form the DAL cluster. The formation of the DAL cluster occurred along with the loss of urate permease (UAP) and urate oxidase (UOX), reducing the requirement for oxygen and bypassing the candidate Ppr1 inducer, uric acid. In Saccharomyces cerevisiae this allantoin catabolism cluster is regulated by the transcription factor Dal82, which is not present in many of the pre-rearrangement fungal species. We have used ChIP-Chip analysis, transcriptional profiling of an activated Ppr1 protein, bioinformatics, and nitrogen utilization studies, to establish that in Candida albicans the zinc cluster transcription factor Ppr1 controls this allantoin catabolism regulon. Intriguingly, in S. cerevisiae the Ppr1 ortholog binds the same DNA motif (CGG(N6)CCG) as in C. albicans, but serves as a regulator of pyrimidine biosynthesis. This transcription factor rewiring appears to have taken place at the same phylogenetic step as the formation of the rearranged DAL cluster. This transfer of the control of allantoin degradation from Ppr1 to Dal82, together with the repositioning of Ppr1 to the regulation of pyrimidine biosynthesis, may have resulted from a switch to a metabolism that could exploit hypoxic conditions in the lineage leading to S. castellii and S. cerevisiae.

Dataset Information

Comprehensive Evaluation of Anti-hyperuricemic Effect of Red Kidney Bean Anthocyanins and Molecular Screening of the Lead Candidate

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