Inflammaging and Vascular Function in Metabolic Syndrome: The Role of Hyperuricemia

Laučytė-Cibulskienė, Agnė; Smaliukaitė, Monika; Dadonienė, Jolanta; Čypiene, A.; Mikolaitytė, Jurgita; Ryliškytė, Ligita; Laucevičius, Aleksandras; Badarienė, Jolita

doi:10.3390/medicina58030373

Cited by 3 publications

(3 citation statements)

References 38 publications

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“…On the other hand, inflammasome-independent inflammatory mechanisms are neutrophils dependent to cause the production of cytokines. Soluble urate inflammatory pathways work in the intracellular environment, where the soluble UA has numerous inflammatory and oxidative actions like intracellular immunometabolic responses, inflammatory responses, free radicals damage, and cell self-consumption [35][36][37][38][39].…”

Section: Discussionmentioning

confidence: 99%

The Cellular Genesis of Metabolic Syndrome and the Role of Anti-urate Drugs in Hyperuricemia Patients: A Systematic Review

Malik,

Ganatra,

Siby

et al. 2024

Cureus

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Hyperuricemia results due to the underexcretion of uric acid through kidneys or overproduction due to either intake of purine-rich foods, a high caloric diet, or a decreased activity of purine recycler hypoxanthine-guanine phosphoribosyl transferase (HGPRT). Increased xanthine oxidoreductase (XOR) enzyme activity may contribute to hyperuricemia. Literature provides growing evidence that an independent component that contributes to the development of metabolic syndrome (MetS) and associated comorbidities is hyperuricemia. Thus, precise cellular mechanisms involved during MetS and related comorbidities in hyperuricemia, and the role of anti-urate medicines in these mechanisms require further investigations. We searched online libraries PubMed and Google Scholar for data collection. We used Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020 guidelines for literature identification, selection, screening, and determining eligibility to produce unbiased meaningful outcomes. We applied quality assessment tools for the quality appraisal of the studies. And, outcomes were extracted from the selected studies, which revealed the relationship between hyperuricemia and MetS components by causing inflammation, endothelial dysfunction, oxidative stress, and endoplasmic reticulum stress. The selected studies reflected the role of xanthine oxide (XO) inhibitors beyond inhibition. This systematic review concluded that hyperuricemia independently causes inflammation, oxidative stress, endothelial damage, and endoplasmic reticulum stress in patients with hyperuricemia. These mechanisms provide a cellular basis for metabolic syndrome and related comorbidities. In this context, XO inhibitors and their beneficial effects go beyond XOR inhibition to ameliorate these pathological mechanisms.

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Section: Discussionmentioning

confidence: 99%

The Cellular Genesis of Metabolic Syndrome and the Role of Anti-urate Drugs in Hyperuricemia Patients: A Systematic Review

Malik,

Ganatra,

Siby

et al. 2024

Cureus

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“…Additionally, C-reactive protein and other cardiovascular damage markers that result from ROS are often elevated compared to normal weight individuals [37]. Furthermore, higher levels of circulating blood lipids and uric acid (hyperuricemia) in the obese, regardless of metabolic status, facilitate damage to both lipids (e.g., nitrosylated lipoproteins) and vascular endothelium [38]. However, in the short-term, MHO carries comparatively lower risks of ROS generation and these patients can more easily undergo exercise and diet interventions to further reduce oxidative stress generated by obesity.…”

Section: Damage From Reactive Oxygen Speciesmentioning

confidence: 99%

Factors of Obesity and Metabolically Healthy Obesity in Asia

2022

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The East Asian region (China, Japan, and South Korea) is comprised of almost 1.5 billion people and recent industrialization has brought with it a pandemic of rising obesity, even in children. As these countries are rapidly aging and functioning at sub-replacement birthrates, the burgeoning costs of obesity-related care may threaten socialized healthcare systems and quality of life. However, a condition called metabolically healthy obesity (MHO) has been found to be without immediate cardiopulmonary or diabetic risk. Thus, maintenance of the MHO condition for the obese in East Asia could buffer the burden of long-term obesity care on medical systems and knowledge of the biochemical, genetic, and physiological milieu associated with it could also provide new targets for intervention. Diverse physiological, psychological, environmental, and social factors play a role in obesogenesis and the transition of MHO to a metabolically unhealthy obesity. This review will give a broad survey of the various causes of obesity and MHO, with special emphasis on the East Asian population and studies from that region.

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“…Hyperuricemia (HUA) is resulted from reduced uric acid excretion or abnormal purine metabolism and is inextricably linked to chronic kidney disease 1 , metabolic syndrome 2 , and type 2 diabetes 3 . A study found that HUA prevalence is 13.5% (17.3% in men, 10.0% in women) when age and sex are standardized 3 .…”

Section: Introductionmentioning

confidence: 99%

The effect of lipid metabolism disorder on patients with hyperuricemia using Multi-Omics analysis

Ma,

Wang,

et al. 2023

Sci Rep

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A multiomics study was conducted to investigate how lipid metabolism disorders affect the immune system in Xinjiang patients with hyperuricemia. The serum of 60 healthy individuals and 60 patients with hyperuricemia was collected. This study used LC–MS and HPLC to analyze differential lipid metabolites and enrichment pathways. It measured levels of immune factors tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6), carnitine palmitoyltransferase-1 (CPT1), transforming growth factor-β1 (TGF-β1), glucose (Glu), lactic acid (LD), interleukin 10 (IL-10), and selenoprotein 1 (SEP1) using ELISA, as well as to confirm dysregulation of lipid metabolism in hyperuricemia. 33 differential lipid metabolites were significantly upregulated in patients with hyperuricemia. These lipid metabolites were involved in arachidonic acid metabolism, glycerophospholipid metabolism, linoleic acid metabolism, glycosylphosphatidylinositol (GPI)—anchor biosynthesis, and alpha-Linolenic acid metabolism pathways. Moreover, IL-10, CPT1, IL-6, SEP1, TGF-β1, Glu, TNF-α, and LD were associated with glycerophospholipid metabolism. In patients with hyperuricemia of Han and Uyghur nationalities, along with healthy individuals, significant differences in CPT1, TGF-β1, Glu, and LD were demonstrated by ELISA (P < 0.05). Furthermore, the levels of SEP1, IL-6, TGF-β1, Glu, and LD differed considerably between groups of the same ethnicity (P < 0.05). It was found that 33 kinds of lipid metabolites were significantly different in patients with hyperuricemia, which mainly involved 5 metabolic pathways. According to the results of further studies, it is speculated that CPT1, TGF-β1, SEP1, IL-6, Glu and LD may increase fatty acid oxidation and mitochondrial oxidative phosphorylation in patients through glycerophospholipid pathway, reduce the rate of glycolysis, and other pathways to change metabolic patterns, promote different cellular functions, and thus affect the disease progression in patients with hyperuricemia.

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Inflammaging and Vascular Function in Metabolic Syndrome: The Role of Hyperuricemia

Cited by 3 publications

References 38 publications

The Cellular Genesis of Metabolic Syndrome and the Role of Anti-urate Drugs in Hyperuricemia Patients: A Systematic Review

The Cellular Genesis of Metabolic Syndrome and the Role of Anti-urate Drugs in Hyperuricemia Patients: A Systematic Review

Factors of Obesity and Metabolically Healthy Obesity in Asia

The effect of lipid metabolism disorder on patients with hyperuricemia using Multi-Omics analysis

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