Serum Uric Acid and 1-h Postload Glucose in Essential Hypertension

Perticone, Francesco; Sciacqua, Angela; Perticone, Maria; Arturi, Franco; Scarpino, Paola Elisa; Quero, Michele; Sesti, Giorgio

doi:10.2337/dc11-1727

Cited by 39 publications

(21 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Furthermore, we also demonstrated that SUA levels had significant impact on the development of diabetes in patients with IFG and/or IA1c, since 1-SD (1.53 mg/dl) increment in SUA signaled a 36% higher risk for type 2 diabetes. Interestingly, a recent study also showed that SUA was strongly associated with 1-h PG in hypertensive NGT individuals, and similar finding could also be observed in hypertensive IGT and diabetes [29]. Our study, together with above mentioned studies, indicated that SUA might be a major determinant of 2-h PG in patients with prediabetes, suggesting the crucial role of SUA in the deterioration of glucose tolerance.…”

Section: Discussionsupporting

confidence: 89%

Association of Serum Uric Acid with 2-Hour Postload Glucose in Chinese with Impaired Fasting Plasma Glucose and/or HbA1c

et al. 2013

View full text Add to dashboard Cite

ObjectiveTo examine whether serum uric acid (SUA) is associated with 2-hour postload glucose (2-h PG) in Chinese with impaired fasting plasma glucose (IFG) and/or HbA1c (IA1C).Research Design and MethodsAnthropometric and biochemical examinations, such as SUA concentration, were performed in 3763 individuals from all the villages in Baqiao County, China. A 75-g oral glucose tolerance test (OGTT) was conducted in 1197 Chinese with prediabetes as having IFG (110≤ fasting plasma glucose [FPG] <126 mg/dl and HbA1c <6.5%), IA1C (5.7% ≤ HbA1c <6.5% and FPG <126 mg/dl), or both.ResultsThe present study included 1197 participants with IFG and/or IA1C (mean age 56.5±10.3 years; 50.6% men). In multivariate linear regression, after adjustment for gender, age, smoking and drinking, body mass index (BMI), systolic and diastolic blood pressure (SBP, DBP), lipid profiles, logarithmic transformed C-reactive protein (log-CRP), estimated glomerular filtration rate (e-GFR), FPG and HbA1c, with a 1-mg/dl increment of SUA, 2-h PG increased by 5.04±0.72 (P<0.001), 3.06±1.08 (P = 0.001), 5.40±1.26 (P<0.001), and 2.34±2.16 mg/dl (P = 0.056) in all participants, in participants with normal glucose tolerance (NGT), with impaired glucose tolerance (IGT), and with 2-h newly diagnosed diabetes (2-h NDM, with 2-h PG ≥200 mg/dl), respectively. In both men and women, 2-h PG increased progressively and significantly from the lower to the upper SUA tertiles (P<0.001). Moreover, in multivariate logistic regression, 1-standard deviation (SD; 1.53 mg/dl) increment of SUA was significantly associated with a 36% higher risk for 2-h NDM (Odds ratio [CI 95%]: 1.36 [1.09–1.99]; P = 0.03).ConclusionsSUA is significantly associated with 2-h PG in Chinese with IFG and/or IA1C.

show abstract

Section: Discussionsupporting

confidence: 89%

Association of Serum Uric Acid with 2-Hour Postload Glucose in Chinese with Impaired Fasting Plasma Glucose and/or HbA1c

et al. 2013

View full text Add to dashboard Cite

show abstract

“…Additionally, in hypertensive participants with normal glucose tolerance tests, uric acid is associated with 1-hour post-load glucose 12 . Thus, we decided to analyze the association of uric acid lowering on HOMA-IR, as a possible intermediate in the development of endothelial dysfunction.…”

Section: Methodsmentioning

confidence: 99%

Effect of Uric Acid–Lowering Agents on Endothelial Function

et al. 2017

View full text Add to dashboard Cite

Higher levels of serum uric acid are independently associated with endothelial dysfunction, a mechanism for incident hypertension. Obese/overweight individuals are more prone to endothelial dysfunction than their lean counterparts. However, the effect of lowering serum uric acid on endothelial dysfunction in these individuals has not been examined thoroughly. In this randomized, double-blind, placebo-controlled trial of nonhypertensive, overweight or obese individuals with higher serum uric acid (body mass index≥25 kg/m2 and serum uric acid≥5.0 mg/dL), we assigned subjects to probenecid (500 to 1000mg/day), allopurinol (300 to 600mg/day), or matching placebo. The primary outcome was endothelial-dependent vasodilation measured by brachial artery ultrasound at baseline and 8 weeks. By the end of the trial, 47, 49 and 53 participants had been allocated to receive probenecid, allopurinol, and placebo, respectively. Mean serum uric acid levels significantly decreased in the probenecid (from 6.1 to 3.5 mg/dL) and allopurinol groups (from 6.1 to 2.9 mg/dL), but not in the placebo group (6.1 to 5.6 mg/dL). None of the interventions produced any significant change in endothelial-dependent vasodilation (probenecid, 7.4±5.1% at baseline and 8.3±5.1% at 8 weeks; allopurinol, 7.6±6.0% at baseline and 6.2±4.8% at 8 weeks; placebo, 6.5±3.8% at baseline and 7.1±4.9% at 8 weeks). In this randomized, double-blind, placebo-controlled trial, uric acid lowering did not impact endothelial function in overweight or obese non-hypertensive individuals. These data do not support the hypothesis that uric acid is causally related to endothelial dysfunction, a potential mechanism for development of hypertension.

show abstract

“…UA is responsible for approximately 50% of serum antioxidant activity [2, 4]. However, in vivo and cellular studies have demonstrated that depending on its chemical microenvironment, UA may also be a pro-oxidant [8]. Strong epidemiological evidence suggests that the prevalence of gout and hyperuricemia is increasing worldwide [9].…”

Section: Introductionmentioning

confidence: 99%

Aldose reductase mediates endothelial cell dysfunction induced by high uric acid concentrations

et al. 2017

View full text Add to dashboard Cite

BackgroundUric acid (UA) is an antioxidant found in human serum. However, high UA levels may also have pro-oxidant functions. According to previous research, aldose reductase (AR) plays a vital role in the oxidative stress-related complications of diabetes. We sought to determine the mechanism by which UA becomes deleterious at high concentrations as well as the effect of AR in this process.MethodEndothelial cells were divided into three groups cultured without UA or with 300 μM or 600 μM UA. The levels of total reactive oxygen species (ROS), of four ROS components, and of NO and NOX4 expression were measured. Changes in the above molecules were detected upon inhibiting NOX4 or AR, and serum H2O2 and vWF levels were measured in vivo.ResultsIncreased AR expression in high UA-treated endothelial cells enhanced ROS production by activating NADPH oxidase. These effects were blocked by the AR inhibitor epalrestat. 300 μM UA decreased the levels of the three major reactive oxygen species (ROS) components: O2•-, •OH, and 1O2. However, when the UA concentration was increased, both O2•- levels and downstream H2O2 production significantly increased. Finally, an AR inhibitor reduced H2O2 production in hyperuricemic mice and protected endothelial cell function.ConclusionsOur findings indicate that inhibiting AR or degrading H2O2 could protect endothelial function and maintain the antioxidant activities of UA. These findings provide new insight into the role of UA in chronic kidney disease.Electronic supplementary materialThe online version of this article (doi:10.1186/s12964-016-0158-6) contains supplementary material, which is available to authorized users.

show abstract

Serum Uric Acid and 1-h Postload Glucose in Essential Hypertension

Cited by 39 publications

References 35 publications

Association of Serum Uric Acid with 2-Hour Postload Glucose in Chinese with Impaired Fasting Plasma Glucose and/or HbA1c

Association of Serum Uric Acid with 2-Hour Postload Glucose in Chinese with Impaired Fasting Plasma Glucose and/or HbA1c

Effect of Uric Acid–Lowering Agents on Endothelial Function

Aldose reductase mediates endothelial cell dysfunction induced by high uric acid concentrations

Contact Info

Product

Resources

About