Fructose Intake, Serum Uric Acid, and Cardiometabolic Disorders: A Critical Review.

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Term Occurence Count Dictionary
febuxostat 1 endocrinologydiseasesdrugs
hyperinsulinemia 1 endocrinologydiseases
hyperuricemia 13 endocrinologydiseases
metabolic syndrome 6 endocrinologydiseases
obesity 9 endocrinologydiseases
vascular calcification 1 endocrinologydiseases
allopurinol 5 endocrinologydiseasesdrugs

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Select Drug Character Offset Drug Term Instance
allopurinol 4181 raises serum UA levels [[11]]. Indeed, several clinical studies have shown that the administration of allopurinol , a competitive antagonist of XO, can significantly improve endothelial function and the circulating
allopurinol 6926 active metabolites oxypurinol act as competitive antagonists of XO and can lower UA levels. In addition, allopurinol has consistently been reported to prevent H2O2 production [[12],[18]] (Figure 1B). Most UA is filtered
allopurinol 16361 In this regard, ROS generation and vascular endothelial dysfunction can be reduced by drugs such as allopurinol and febuxostat, which inhibit XO activity and consequently reduce UA production [[80]].OONO− is a
allopurinol 23103 XO inhibition could benefit patients with high circulating UA levels, focusing on the XO inhibitor allopurinol and its active metabolite oxypurinol. Allopurinol has displayed beneficial effects on blood pressure
allopurinol 26553 production of the superoxide anion (O2−) and hydrogen peroxide (H2O2). The competitive antagonist allopurinol is converted in the active form, oxypurinol, via XO activity, acting as an XO inhibitor; (B) During
febuxostat 16377 ROS generation and vascular endothelial dysfunction can be reduced by drugs such as allopurinol and febuxostat , which inhibit XO activity and consequently reduce UA production [[80]].OONO− is a potent non-radical
Select Disease Character Offset Disease Term Instance
hyperinsulinemia 9730 secondary phenomenon in metabolic syndrome, it is also an independent predictive factor for obesity and hyperinsulinemia [[4]]. In themselves, UA accumulation and lack of vitamin C do not cause obesity. Rather, they increase
hyperuricemia 970 final product of purine metabolism. Recent preclinical and clinical evidence suggests that chronic hyperuricemia is an independent risk factor for hypertension, metabolic syndrome, and cardiovascular disease. It is
hyperuricemia 2777 UA levels are higher in Western countries than in the rest of the world. In non-Western countries, hyperuricemia is relatively rare in rural communities. However, there is increased migration from rural areas to cities
hyperuricemia 2951 increased migration from rural areas to cities or communities where the Western diet is dominant and hyperuricemia is more prevalent [[7]].Recent research suggests that hyperuricemia may be caused by elevated activity
hyperuricemia 3019 the Western diet is dominant and hyperuricemia is more prevalent [[7]].Recent research suggests that hyperuricemia may be caused by elevated activity of the enzyme xanthine oxidase (XO) [[8]]. Xanthine oxidase inhibitors
hyperuricemia 3705 great apes are at least 10 times higher than in other mammals, with the consequent risk of developing hyperuricemia [[9]]. High UA levels favor adipose tissue formation, which was originally an evolutionary advantage
hyperuricemia 4800 (including Scopus, Google Scholar, PubMed, and Web of Science) for peer-reviewed studies focusing on XO, hyperuricemia , fructose, and CVD. The search strategy was designed to retrieve studies published in English from journal
hyperuricemia 7277 eliminated in faeces. Inefficient renal excretion of UA is the main cause of both primary and secondary hyperuricemia [[19]]. Renal UA excretion is regulated by several transporters. Renal UA reabsorption is mediated by
hyperuricemia 9584 correlation between circulating UA and obesity, especially visceral obesity [[44]]. Accordingly, although hyperuricemia is often considered to be a secondary phenomenon in metabolic syndrome, it is also an independent predictive
hyperuricemia 20417 These findings also demonstrate that decreased urinary UA excretion may contribute to fructose-induced hyperuricemia . This mechanism could substantially increase the risk of gout in people who consume high amounts of
hyperuricemia 20693 onset of metabolic syndrome and increases insulin resistance [[51]].Many experiments have shown that hyperuricemia may have a potential role in endothelial dysfunction and reduced NO bioavailability. However, several
hyperuricemia 21234 say whether UA is a causal, compensatory, or coincidental factor for CVD [[104]]. Generally, gout and hyperuricemia patients also suffer from hypertension, CKD, insulin resistance, and obesity [[105]]. However, no clear
hyperuricemia 24758 evaluated [[121],[122]].7. ConclusionsIn summary, a specific causal link between fructose consumption, hyperuricemia , and CVD has not yet been established. There is an association between UA and established cardiovascular
hyperuricemia 26034 useful tools for predicting the potential effects of new XO inhibitors, which could be used to treat hyperuricemia linked with cardiometabolic disorders.Figure 1Uric acid formation through xanthine oxidase activity.
metabolic syndrome 1032 clinical evidence suggests that chronic hyperuricemia is an independent risk factor for hypertension, metabolic syndrome , and cardiovascular disease. It is probably also an independent risk factor for chronic kidney disease,
metabolic syndrome 3321 Both are risk factors for gout, chronic kidney disease (CKD), CVD, obesity, insulin resistance, and metabolic syndrome . Humans and great apes produce UA via XO-catalyzed oxidation of purines. Unlike other mammals, humans
metabolic syndrome 9650 obesity [[44]]. Accordingly, although hyperuricemia is often considered to be a secondary phenomenon in metabolic syndrome , it is also an independent predictive factor for obesity and hyperinsulinemia [[4]]. In themselves,
metabolic syndrome 18031 risk. Hyperuricemia is increasing in prevalence, as are its associated pathological conditions, such as metabolic syndrome , CKD, and CVD [[8],[89]]. The average serum UA levels in the general population are rising [[90]] due
metabolic syndrome 20601 people who consume high amounts of fructose. Moreover, chronic exposure to fructose favours the onset of metabolic syndrome and increases insulin resistance [[51]].Many experiments have shown that hyperuricemia may have a potential
metabolic syndrome 22848 causal link between dietary fructose intake and metabolic disorders, such as obesity, diabetes, and metabolic syndrome . However, while some studies have found a link, other studies have not [[114]].Recent relevant clinical
obesity 3288 reducing UA and oxidative stress. Both are risk factors for gout, chronic kidney disease (CKD), CVD, obesity , insulin resistance, and metabolic syndrome. Humans and great apes produce UA via XO-catalyzed oxidation
obesity 3939 Nowadays, however, excess adipose tissue is considered a predisposing factor for insulin resistance, obesity , and hypertension [[10]]. This excessive fat storage may be due to increased consumption of fructose-enriched
obesity 9517 fail to gain fat [[41],[42],[43]]. Thus, there is a positive correlation between circulating UA and obesity , especially visceral obesity [[44]]. Accordingly, although hyperuricemia is often considered to be a
obesity 9546 [[41],[42],[43]]. Thus, there is a positive correlation between circulating UA and obesity, especially visceral obesity [[44]]. Accordingly, although hyperuricemia is often considered to be a secondary phenomenon in metabolic
obesity 9718 to be a secondary phenomenon in metabolic syndrome, it is also an independent predictive factor for obesity and hyperinsulinemia [[4]]. In themselves, UA accumulation and lack of vitamin C do not cause obesity.
obesity 9820 obesity and hyperinsulinemia [[4]]. In themselves, UA accumulation and lack of vitamin C do not cause obesity . Rather, they increase susceptibility to obesity and diabetes as a result of an interaction between
obesity 9869 UA accumulation and lack of vitamin C do not cause obesity. Rather, they increase susceptibility to obesity and diabetes as a result of an interaction between genetic factors (mostly a polygenic contribution)
obesity 21317 Generally, gout and hyperuricemia patients also suffer from hypertension, CKD, insulin resistance, and obesity [[105]]. However, no clear link has yet been demonstrated between a HFrD and CVD. A recent systematic
obesity 22825 have attempted to prove a causal link between dietary fructose intake and metabolic disorders, such as obesity , diabetes, and metabolic syndrome. However, while some studies have found a link, other studies have
vascular calcification 15126 resistance and imbalance in vascular homeostasis, including endothelial cell dysfunction, atherosclerosis, vascular calcification , and impaired myocardial energetics, stimulating the production of interleukin-1 (IL-1), interleukin-6

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