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Hyperuricemia Predisposes to the Onset of Diabetes

ABSTRACT: To further examine the mechanisms of urate in islet β-cell death, we have employed whole genome microarray expression profiling as a discovery platform to identify genes with the potential to distinguish primacy of streptozotocin (STZ) vs. urate. Islets were isolated from Uox-KO and WT mice with and without multiple low-dose STZ. Differentially expressed genes (DEGs) in islets of the hyperuricemic and/or diabetic mice in comparison to their respective controls represented specific Gene Ontology (GO) pathways and Kyoto Encyclopedia of Genes and Genomes (KEGG) functional meanings.

ORGANISM(S): Mus musculus

PROVIDER: GSE142421 | GEO | 2020/05/04

REPOSITORIES: GEO

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Hyperuricemia Predisposes to the Onset of Diabetes

Project description:Hyperuricemia Predisposes to the Onset of Diabetes

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Project description:Clinical studies have shown a link between hyperuricemia (HU) and diabetes, while the exact effect of soluble serum urate on glucose metabolism remains elusive. This study aims to characterize the glucose metabolic phenotypes and investigate the underlying molecular mechanisms using a novel spontaneous HU mouse model in which the uricase (Uox) gene is absent. In an attempt to study the role of HU in glycometabolism, we implemented external stimulation on Uox knockout (KO) and wild-type (WT) males with a high-fat diet (HFD) and/or injections of multiple low-dose streptozotocin (MLD-STZ) to provoke the potential role of urate. Notably, while Uox-KO mice developed glucose intolerance in the basal condition, no mice spontaneously developed diabetes, even with aging. HFD-fed Uox-KO mice manifested similar insulin sensitivity compared with WT controls. HU augmented the existing glycometabolism abnormality induced by MLD-STZ and eventually led to diabetes, as evidenced by the increased random glucose. Reduced β-cell masses and increased terminal deoxynucleotidyl TUNEL-positive β-cells suggested that HU-mediated diabetes was cell death dependent. However, urate-lowering therapy (ULT) cannot ameliorate the diabetes incidence or reverse β-cell apoptosis with significance. ULT displayed a significant therapeutic effect of HU-crystal-associated kidney injury and tubulointerstitial damage in diabetes. Moreover, we present transcriptomic analysis of isolated islets, using Uox-KO versus WT mice and streptozotocin-induced diabetic WT (STZ-WT) versus diabetic Uox-KO (STZ-KO) mice. Shared differentially expressed genes of HU primacy revealed Stk17β is a possible target gene in HU-related β-cell death. Together, this study suggests that HU accelerates but does not cause diabetes by inhibiting islet β-cell survival.

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Project description:Objective: Our study aimed to evaluate differences in plasma lipidome between patients with asymptomatic hyperuricemia (HUA) detected < 40 years (HUA<40) and > 40 years, gout patients with disease onset < 40 years (Gout<40) and > 40 years, and normouricemic healthy controls. Methods: Plasma samples were collected from 94 asymptomatic HUA (77% HUA<40) subjects, 196 gout patients (59% Gout<40), and 70 normouricemic controls. A comprehensive targeted lipidomic analysis was performed to semi-quantify 608 lipids in plasma. Univariate and multivariate statistics and advanced visualizations were applied. Results: Both HUA and gout patients showed similar changes in lipid profiles with the highest upregulation of phosphatidylethanolamines (median fold-changes and p-values were 2.9/3.4 and p=1.5x10-16/p=5.5x10-21 for HUA/Gout, respectively) and downregulation of lysophosphatidylcholine plasmalogens/plasmanyls (median fold-changes and p-values were 0.3/0.5 and p=4.8x10-21/p=2.2x10-21 for HUA/Gout, respectively). More profound changes were observed in HUA<40 and Gout<40. Moreover, a shift in the lipid profile towards controls was apparent in HUA<40 and Gout<40 during urate-lowering treatment. Multivariate statistics differentiated HUA<40 and Gout<40 groups from controls with an overall accuracy of > 94%. Conclusion: The changes in the lipidome of HUA and Gout patients show a significant impact on lipid metabolism and a severe pathobiochemical effect, with no relationship with common determinants such as body mass index, metabolic syndrome, or pathogenic variants in major urate transporter ABCG2. The most significant glycerophospholipid dysregulation was found in HUA<40 and Gout<40 patients, together with a correction of this imbalance with urate-lowering treatment.

2023-03-30 | MSV000091596 | MassIVE

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