Serum Uric Acid Concentration Research Articles

A review on the fruit components affecting uric acid level and their underlying mechanisms.

Uric acid (UA) is produced in the liver and excreted through the kidneys and intestines. If UA is overproduced or its excretion reduces, the concentration of UA increases, leading to hyperuricemia and gout. The high concentration of UA is also related to cardiovascular disease, hypertension, obesity, and other diseases. Fruits are healthy foods. However, fruits contain fructose and small amounts of purine, and the product of their metabolism is UA. Therefore, theoretically, eating fruits will increase the concentration of serum UA. Fruit components are numerous, and their effects on serum UA are complex. According to the current research, fructose, purine, polyphenols, vitamin C, dietary fiber, and minerals present in fruits influence serum UA concentrations. In addition to the UA synthesized by fructose and purine metabolism, the mechanisms by which other components affect the concentration of serum UA can be summarized as follows: (a) inhibiting xanthine oxidase; (b) reducing reabsorption of UA; and (c) improving the excretion of UA. In this review, we comprehensively discussed the fruit components that affect serum UA concentrations, and explained their mechanisms for the first time, which references for patients with hyperuricemia to take fruits. PRACTICAL APPLICATIONS: With the rising prevalence, hyperuricemia and gout have become public health problems that endanger our daily life. The key to the treatment of hyperuricemia is to control the level of serum UA within the normal range. Fruits are healthy foods. However, fruit components are numerous, and their effects on serum UA are complex. According to the current research, fructose, purine, polyphenols, vitamin C, dietary fiber, and minerals present in fruits influence serum UA concentrations. In this review, we comprehensively discussed the fruit components that affect serum UA concentrations. We also explained their mechanisms, which references for patients with hyperuricemia to take fruits.

Prevalence of hyperuricemia in cerebrovascular accidents and its correlation with their outcome

Introduction: Cerebrovascular accident or stroke is a disease of the vascular system of the brain.According to ICD 11, stroke is classified as a neurological disease and not under the circulatorysystem. It is the second leading cause of death worldwide. It cannot be said that high Serum UricAcid [SUA] amongst patients with cerebrovascular accidents is directly correlated with theiroutcome. The present study planned to estimate uric acid levels and their association in acute strokepatients, both ischemic and hemorrhagic. Method: A total of 100 stroke patients admitted under theneurology department were included in the study. Brain imaging (CT/MRI) was performed. Theserum uric acid was estimated. Results: Out of a total of 100 patients, 74 were males, and 26 werefemales. Nine patients were less than 45 years old and 91 patients were 45 and above. Thirty-ninepatients had ischemic, and 61 patients had a hemorrhagic stroke, respectively. Out of 100 patients,23 patients had normal uric acid levels (<7mg/dl). Seventy-seven patients were with high uric acidlevels. The mean serum uric acid concentration in male patients was 8.48±2.7and 9.20±2.7 infemales. Among the total 100 cases, 69 survived, and the remaining 31 were among the non-survivor group at the time of discharge. Mean serum uric acid in stroke survivors was 8.5±2.6mg/dl, while in non-survivors, it was 8.6±2.2 mg/dl. There was no significant difference between thelevels of uric acid among survivors and non-survivors. Conclusions: The prevalence ofhyperuricemia (>9mg/dl) amongst stroke patients was 77% in the present study. The values ofserum uric acid were significantly elevated in the patients aged > 45 years. The serum uric acidvalues were high among the group of hyperglycemic and hypertensive patients at the time ofadmission. There was no significant difference between the levels of uric acid among survivors andnon-survivors.

Hyperuricemia-induced endothelial insulin resistance: the nitric oxide connection.

Hyperuricemia, defined as elevated serum concentrations of uric acid (UA) above 416µmol L-1, is related to the development of cardiometabolic disorders, probably via induction of endothelial dysfunction. Hyperuricemia causes endothelial dysfunction via induction of cell apoptosis, oxidative stress, and inflammation; however, it's interfering with insulin signaling and decreased endothelial nitric oxide (NO) availability, resulting in the development of endothelial insulin resistance, which seems to be a major underlying mechanism for hyperuricemia-induced endothelial dysfunction. Here, we elaborate on how hyperuricemia induces endothelial insulin resistance through the disruption of insulin-stimulated endothelial NO synthesis. High UA concentrations decrease insulin-induced NO synthesis within the endothelial cells by interfering with insulin signaling at either the receptor or post-receptor levels (i.e., proximal and distal steps). At the proximal post-receptor level, UA impairs the function of the insulin receptor substrate (IRS) and phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) in the insulin signaling pathway. At the distal level, high UA concentrations impair endothelial NO synthase (eNOS)-NO system by decreasing eNOS expression and activity as well as by direct inactivation of NO. Clinically, UA-induced endothelial insulin resistance is translated into impaired endothelial function, impaired NO-dependent vasodilation, and the development of systemic insulin resistance. UA-lowering drugs may improve endothelial function in subjects with hyperuricemia.

Sodium-glucose co-transporter 2 inhibitors in heart failure with preserved ejection fraction: reasons for optimism.

Sodium-glucose co-transporter 2 inhibitors in heart failure with preserved ejection fraction: reasons for optimism.

Antihyperuricemic Effect of Dendropanax morbifera Leaf Extract in Rodent Models.

Dendropanax morbifera is a well-known traditional medicine used in China and Korea to treat intestinal disorders, urosis, diuresis, and chronic glomerulonephritis. Hyperuricemia is a metabolic disorder characterized by a high uric acid level in serum due to an imbalance between uric acid production and excretion and causes gout. Recently, the prevalence of hyperuricemia worldwide has been continuously increasing. Xanthine oxidase (XOD) inhibitors (allopurinol (ALP) and febuxostat) and uricosuric agents (benzbromarone and probenecid) are used to treat hyperuricemia clinically. However, because these drugs are poorly tolerated and cause side effects, such as kidney diseases, hepatotoxicity, gastrointestinal symptoms, and hypersensitivity syndrome, only a limited number of drugs are available. We investigated the antihyperuricemic effects of Dendropanax morbifera leaf ethanol extract (DMLE) and its underlying mechanisms of action through in vitro and in vivo studies. We evaluated uric acid levels in serum and urine, and xanthine oxidase (XOD) inhibition activity in the serum and liver tissue of a hyperuricemic rat model of potassium oxonate (PO)-induced hyperuricemic rats. In vitro study, XOD-inhibitory activity was the lowest among the test substances at the IC50 of ALP. However, the IC50 of DMLE-70 was significantly low compared with that of other DMLEs (p < 0.05). In PO-induced hyperuricemic rats, uric acid (UA) levels in serum and urine were significantly reduced in all DMLE-70 and allopurinol-treated (ALT) groups than in the PC group (p < 0.05). UA levels in urine were lower than those in serum in all DME groups. In PO-induced hyperuricemic rats, DMEE-200 reduced UA concentration in serum and increased UA excretion in the urine. These findings suggest that DMLE exerts antihyperuricemic and uricosuric effects on promoting UA excretion by enhanced secretion and inhibition of UA reabsorption in the kidneys. Thus, DMLE may be a potential treatment for hyperuricemia and gout.

Сечокам'яна хвороба як наслідок вторинної гіперурикемії у пацієнтів з діабетичним ураженням нирок

Urolithiasis is currently one of the most pressing problems of modern urology and medicine in general. The pathogenesis of urolithiasis is multifactorial and caused by various metabolic disorders, in particular carbohydrate, the main manifestation of which is diabetes mellitus. In connection with the above, a comparative approach to the study of metabolic disorders in patients with diabetic kidney damage, in particular hyperuricemia, is relevant in order to identify possible causes of lithogenesis. The purpose of the study is to study the effect of secondary hyperuricemia on the formation of urinary stones in patients with diabetic kidney damage, compared with non-diabetic nephropathies. Materials and methods. The study included 59 patients with chronic kidney disease, including 27 with diabetic nephropathy and 32 with non-diabetic nephropathy. All patients underwent a comprehensive clinical and laboratory study, which included glycosylated hemoglobin, glycemic profile, lipid complex, C-reactive protein, serum creatinine, urea, electrolytes, uric acid, uric acid clearance, glomerular filtration rate, and ultrasound examination of the urinary system. Results and discussion. Urolithiasis was detected in 70.3 % patients with diabetic kidney disease and in 29.6% patients with non-diabetic pathology. The stones had a renal localization: pelvic stones occurred in 38.9% patients, stones in calyces – in 61.1% patients. When assessing the biochemical parameters, the average level of uric acid in the blood serum of patients with diabetes mellitus significantly exceeded the same indicator in the group of patients with non-diabetic pathology. Also, the level of hyperuricemia was higher in diabetic patients with a glycosylated hemoglobin content of more than 8.5%, compared with patients with an HbA1 concentration of less than 7.5%. In patients of both groups compared with serum uric acid concentrations exceeding the level of 498.5 mmol/l in men and 384.2 mmol/L in women, there was a progression of arterial hypertension. In patients with diabetic nephropathy, there was a significant increase in the level of cholesterol, low-density lipoproteins and triglycerides, which provided an increase in the value of the atherogenicity index to 5.7±1.2. Conclusion. In patients with diabetic kidney damage, there are prerequisites for the development of urolithiasis, due to the development of a number of metabolic disorders that affect kidney function and the composition of urine. The key links in the pathogenesis of more frequent development of urolithiasis in this category of patients are secondary hyperuricemia, as well as disorders of carbohydrate and lipid metabolism in the form of hyperglycemia and hyperlipidemia

A study of the association of serum uric acid levels with alanine aminotransferase and gamma-glutamyl transferase levels in non-alcoholic fatty liver disease patients diagnosed by imaging studies

Background: Non-alcoholic fatty liver disease (NAFLD) is a condition defined by excessive fat accumulation in the form of triglycerides (steatosis) in the liver. In recent years, an association between elevated serum uric acid concentrations and NAFLD has been reported. The aim of the study was to perform cross-sectional study to determine the association between serum uric acid levels and the levels of serum alanine aminotransferase (ALT) and gamma-glutamyl transferase (GGT), in NAFLD patients.Methods: In this hospital-based cross-sectional study, 300 patients with diagnosed NAFLD were included during the one-year period from July 2015 to June 2016.Results: Elevation of alanine aminotransferase levels was seen in a total of 93 cases (31%) and elevation of GGT levels in NAFLD patients was seen in 112 patients out of a total of 300 (37.33%). Hyperuricemia was observed in 99 cases out of a total of 300 cases of NAFLD (33%). A significant association was observed between the two parameters.Conclusions: The prevalence rate of NAFLD was significantly higher in subjects with hyperuricemia than that in those without hyperuricemia (78.19% versus 40.83 %) (p&lt;0.001), and the prevalence rate increased with progressively higher serum uric acid levels (p&lt;0.001). The relationship between rising uric acid levels with rising ALT and GGT levels in these patients was also found to be statistically significant.

Studies of the effect of Carbofuran Inbosting kidney of the Channa punctatus (Bloch.)

Water contamination is a big issue on a global scale. It has been stated that it is the leading cause of death and disease on a global scale, responsible for the deaths of thousands of people every day. Numerous pesticides are also a cause of pollution in agriculture, as they are sprayed on crops to protect them against pests and insects. They have an effect on the soil's structure and fertility. The purpose of this study is to determine the toxicity of the pesticide carbofuran on the fish Channa punctatus. The investigation will be conducted in the kidney and will include histopathological and biochemical examinations. The criteria chosen include urea, uric acid, calcium, potassium, sodium, and creatinine, which can result in catastrophic consequences in many fish diseases. Channa punctatus is a common freshwater fish that was gathered from September to October. It is a robust fish that adapts well to aquarium conditions. Carbofuran is a white, crystalline, powdered insecticide that was used for this study. The elevated serum urea, uric acid, and creatinine concentrations in Channa punctatus at different time intervals of 24, 48, 72, and 96 hours in comparison to the control group reflect compromised kidney functions caused by carbofuran poisoning.

Spectrum-effect relationship between high-performance thin-layer chromatography data and xanthine oxidase inhibitory activity of celery seed extract.

Celery seeds are medicinal herbs used for the prevention and treatment of gout as these have the ability to inhibit the activity of xanthine oxidase and reduce the concentration of serum uric acid. In this study, the relationship between xanthine oxidase inhibitory effects and high-performance thin-layer chromatography data of celery seed extracts was established using multilayer neural network (MNN) in combination with principal component analysis (PCA). The constructed MNN-PCA model was stable and had accurate prediction ability with coefficient of determination =0.9998, leave-one-out coefficient =0.7371, root mean square error =0.0025, and mean absolute deviation =0.0019 for the training set and coefficient of determination =0.8124, root mean square error =0.0784, and mean absolute deviation =0.0645 for the test set. This model can be used to identify the main compounds related to the xanthine oxidase inhibitory effect of celery seed extract. These results can be applied not only to celery extract but also to other herbal medicines.

Resveratrol affects the expression of uric acid transporter by improving inflammation.

Resveratrol (RSV), a polyphenol, non-flavonoid plant-derived antitoxin, ameliorates hyperuricemia and kidney inflammation. The present study aimed to establish a model of high-fat diet (HFD)-induced insulin resistance (IR) and to determine the specific mechanism of RSV to improve kidney inflammation and reduce uric acid (UA). C57BL/6J mice were fed a HFD for 12 weeks and their glucose tolerance was evaluated by intraperitoneal glucose tolerance testing. The mice were then administered RSV for 6 weeks, and blood and kidney samples were collected. Serum UA and insulin concentrations were determined using ELISA kits. Hematoxylin and eosin, periodic acid-Schiff and Masson staining were performed to observe the pathological changes of the kidney, and electron microscopy was used to observe changes in the kidney ultrastructure. The renal concentrations of interleukin (IL)-6, IL-18, IL-1β and tumor necrosis factor-α (TNF-α) were measured using ELISA kits, and western blotting evaluated changes in the protein expression levels of various indicators. RSV significantly ameliorated HFD-induced IR and reduced blood UA levels. Long-term IR can lead to lipid deposition, glycogen accumulation, inflammatory damage and fibrotic changes in the kidney of mice. This leads to a significant increase in the expression of UA transport-related proteins, an increase in UA reabsorption and an increase in blood UA levels. Notably, RSV intervention was able to reverse this process. The effect of RSV may be achieved by inhibiting the NOD-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome and Toll-like receptor 4 (TLR4)/myeloid differentiation factor 88/nuclear factor-κB signaling pathway. In conclusion, RSV may improve kidney inflammation through TLR4 and NLRP3 signaling pathways, and reduce the expression of UA transporter proteins in the kidney of insulin-resistant mice, thereby reducing blood UA levels.

Relation Of Serum Uric Acid Concentrations With Etiology And Severity In Patients With Cirrhosis Of Liver

Background: Hyperuricemia is now an established factor to cause oxidative stress, insulin resistance and systemic inflammation. So it is likely that hyperuricemia might be involved in hepatic necro-inflammation and destruction which are the common underlying pathophysiology of cirrhosis. On the other hand, as uric acid is the end product of cellular degradation, increased hepatocyte destruction due to any etiology increases the level of serum uric acid which might further aggravate hepatic necro-inflammation, cirrhosis &amp; complications. Objectives: To assess serum uric acid concentrations in patients of cirrhosis of liver and its relation with cirrhosis of different etiology, disease severity and liver enzymes. Materials and Methods: This cross sectional observational study was carried out in the Department of Gastroenterology, BSMMU, Bangladesh during the period of September 2015 to October 2016. A total of 220 diagnosed cases of cirrhosis of liver due to any cause from inpatient &amp; outpatient Department of Gastroenterology of Banghabandhu Sheikh Mujib Medical University were enrolled as the study population. Serum uric acid level was measured in each patient and its relationship with different etiology of cirrhosis, severity of cirrhosis and liver enzymes were assessed. Results: The mean age was found to be 47.8 ± 14.6 years and male: female ratio was 1.9:1. Majority patients (52.3%) belonged to CTP Class C. The mean (±SD) value of serum uric acid was 6.19 (±3.25mg/dl) and hyperuricemia (&gt;7 mg/dl) was detected in 27.73% patients. Among all etiologies of CLD, the higher mean (±SD) level of serum uric acid was found in NAFLD (19.54 ±2.20 mg/dl). There was positive correlation of serum uric acid with liver enzymes. Conclusion: Mean serum uric acid level increased gradually as the cirrhotic patients progressed to higher CTP classes &amp; there was positive correlation of serum uric acid with liver enzymes. It requires further large scale multicenter studies with increased sample size &amp; prolong follow-up to establish serum uric acid as a risk factor of CLD.

Prevalence of Hyperuricemia and Its Related Risk Factors Among Students in Fangshan District, Beijing, China

Abstract Objectives To study the prevalence of hyperuricemia among students and explore factors related to hyperuricemia. Methods This is a cross-sectional prevalence study in 530 students aged 6 to 13 years old. The study was conducted from October to November 2019 in Fangshan District, Beijing, China. BMI, glucose, cholesterol HDL, triglycerides, cholesterol LDL and uric acid were measured. Results The overall serum uric acid concentrations was 301.7 ± 74.2 μmol/L. The mean serum uric acid concentrations in boys and girls were 311.1 ± 74.2 μmol/L and 311.1 ± 74.2 μmol/L, respectively. The overall prevalence of hyperuricemia (serum uric acid ≥ 416 μmol/L) was 7.0%. Logistic regression showed that hyperuicemia was worse in boys, students who were older and with high BMI. Conclusions The serum acid concentration among students was high, interventions for high-risk students should be taken. Funding Sources Beijing Center for Diseases Control and Prevention.

MO491ASSOCIATION BETWEEN SERUM URIC ACID LEVEL AND CHRONIC KIDNEY DISEASE INCIDENCE STRATIFIED BY SEX IN MIDDLE-AGED ADULTS

Abstract Background and Aims While previous studies have reported the association between serum uric acid (SUA) and chronic kidney disease (CKD) incidence, the sex differences in this association remain controversial. Therefore, we examined the association between SUA levels and CKD incidence in middle-aged adults stratified by sex using data from a large-scale health check-up. Method We analyzed information from the JMDC database, which included the annual health check-up data of Japanese employees and their dependents aged &amp;lt;75 years. Among those individuals, we analyzed data from 138,511 individuals without CKD, kidney disease, or a history of cardiovascular disease at baseline. CKD was defined as an estimated glomerular filtration rate (eGFR) &amp;lt;60 mL/min/1.73 m2 and/or proteinuria. We divided the participants into 9 and 7 groups according to SUA levels for men and women, respectively. A Cox model was applied to assess the adjusted hazard ratios (HRs) for CKD incidence in each SUA level group using an SUA concentration of 4.0–4.9 mg/dL as the reference after adjusting for age, body mass index, current or ex-smoker, current or ex-drinker, diabetes mellitus, dyslipidemia, systolic blood pressure, use of anti-hyperuricemic drugs, and baseline eGFR. Results The mean participant age was 44.1 years, and 29.6% were women. The mean SUA levels were 5.9 mg/dL and 4.1 mg/dL in men and women, respectively. During the mean follow-up period of 4.68 years, 12,589 participants developed CKD. The age-standardized incidence rates for CKD were 17.88/17.80 per 1000 person-years in men/women with SUA concentrations of 4.0–4.9 mg/dL, 209.76 per 1000 person-years in men with SUA ≥11.0 mg/dL, and 73.38 per 1000 person-years in women with SUA ≥ 9.0 mg/dL. The fully adjusted HRs (95% confidence interval [CI], P value) for CKD incidence in the groups with SUA concentrations of &amp;lt;4.0, 10.0–10.9, and ≥11.0 mg/dL compared with those with SUA of 4.0–4.9 mg/dL among men were 1.13 (1.01–1.26, P=0.030), 1.98 (1.32–2.97, P=0.0010), and 3.74 (1.68–8.35, P=0.0013), respectively. In women, the fully adjusted HRs for CKD incidence in the groups with SUA concentrations of &amp;lt;4.0, 8.0–8.9, and ≥9.0 mg/dL were 1.08 (1.01–1.16, P=0.032), 2.39 (1.07–5.35, P=0.034), and 3.20 (0.80–12.8, P=0.10), respectively. Similar results were observed when we performed the sensitivity analysis excluding 8,411 individuals with hypertensive treatment from the main analysis. The HRs for the outcomes caused by the onset of eGFR &amp;lt;60 mL/min/1.73 m2 or proteinuria separately were similar to those for the main results. Conclusion The results of the present study demonstrated an increased risk of CKD in men with SUA concentrations of &amp;lt;4.0 and ≥10.0 mg/dL and &amp;lt;4.0 and ≥8.0 mg/dL in women compared to those with SUA concentrations of 4.0–4.9 mg/dL after adjusting for various covariates. Both high and low SUA levels were risk factors for CKD in middle-aged men and women. Hyperuricemia was demonstrated to cause renal injury due to the intraluminal deposition of uric acid crystals in the renal collecting duct. Hyperuricemia may also induce endothelial dysfunction, activation of the renin-angiotensin system, and induction of inflammation and stimulation of vascular smooth muscle cell proliferation by the induction of cyclooxygenase-2. However, as uric acid is one of the most important antioxidants in human plasma, low SUA levels may increase the risk of CKD incidence through decreased antioxidant activity. These mechanisms are implicated in the pathogenesis of CKD caused by high and low SUA levels. In addition, the SUA levels and ranges associated with increased risks of CKD incidence differed by sex.

Effect of application at Shu-Mu acupoint on serum uric acid in hyperuricemic rats

To observe the effect of application at Back-Shu with Front-Mu acupoints on serum uric acid (SUA) and kidney uric acid transport related proteins in hyperuricemia rats, so as to explore the mechanism of Shu-Mu acupoint application on treatment of hyperuricemia. SD rats were randomly divided into blank control, model, vaseline application and medication application groups, with 8 rats in each group. The hyperuricemia rat model was established by gavage of potassium oxonate. Rats in the vaseline application group received application of vaseline at bilateral "Ganshu"(BL18) and "Qimen"(LI14), "Pishu"(BL20) and "Zhangmen"(LR13), "Shenshu" (BL23) and "Jingmen"(GB25). Rats in the medication application group received application of traditional Chinese medicine at the same acupoints. The contents of SUA and creatinine (SCr) were detected by automatic biochemical analyzer. H.E. staining was used to observe the pathological changes of kidney. And the protein expression levels of organic anion transporter 1(OAT1) and adenosine triphosphate binding cassette transporter G2(ABCG2) were detected by immunohistochemistry. Rats in the model group showed symptoms such as polydipsia, polyuria, loose stools, fatigue, weakness, etc. The renal tubules atrophied, and urate crystals can be seen in the lumen. Compared with the control group. the SUA content in the model group increased (P<0.01)and the expressions of OAT1 and ABCG2 protein in kidney decreased (P<0.01). After intervention and in comparison with the model group showed that, the diet, excretion function, and mental state of the rats in the medication application group returned to normal, and the pathological changes of the kidney tissue were alleviated, the SUA content was down-regulated(P<0.01)and the expression levels of OAT1 and ABCG2 in the kidney up-regulated (P<0.01). There was no statistically significant difference in the SCr content among the 4 groups (P＞0.05). Medication application at Shu-Mu points can effectively reduce the SUA level of hyperuricemia rats, which may be related to its effects in up-regulating the protein expressions of OAT1 and ABCG2 in the kidney and reducing the damage to the kidneys.

Association of serum uric acid concentration with diabetic retinopathy and its severity

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Allopurinol ameliorates high fructose diet induced hepatic steatosis in diabetic rats through modulation of lipid metabolism, inflammation, and ER stress pathway

Excess fructose consumption contributes to development obesity, metabolic syndrome, and nonalcoholic fatty liver disease (NAFLD). Uric acid (UA), a metabolite of fructose metabolism, may have a direct role in development of NAFLD, with unclear mechanism. This study aimed to evaluate role of fructose and UA in NAFLD and explore mechanisms of allopurinol (Allo, a UA lowering medication) on NAFLD in Otsuka Long-Evans Tokushima Fatty (OLETF) rats fed a high fructose diet (HFrD), with Long-Evans Tokushima Otsuka (LETO) rats used as a control. There were six groups: LETO, LETO-Allo, OLETF, OLETF-Allo, OLETF-HFrD, and OLETF-HFrD-Allo. HFrD significantly increased body weight, epididymal fat weight, and serum concentrations of UA, cholesterol, triglyceride, HbA1c, hepatic enzymes, HOMA-IR, fasting insulin, and two hour-glucose after intraperitoneal glucose tolerance tests, as well as NAFLD activity score of liver, compared to the OLETF group. Allopurinol treatment significantly reduced hepatic steatosis, epididymal fat, serum UA, HOMA-IR, hepatic enzyme levels, and cholesterol in the OLETF-HFrD-Allo group. Additionally, allopurinol significantly downregulated expression of lipogenic genes, upregulated lipid oxidation genes, downregulated hepatic pro-inflammatory cytokine genes, and decreased ER-stress induced protein expression, in comparison with the OLETF-HFrD group. In conclusion, allopurinol ameliorates HFrD-induced hepatic steatosis through modulation of hepatic lipid metabolism, inflammation, and ER stress pathway. UA may have a direct role in development of fructose-induced hepatic steatosis, and allopurinol could be a candidate for prevention or treatment of NAFLD.

Serum Uric Acid Concentrations and Risk of Adverse Outcomes in Patients With COVID-19.

BackgroundAlthough hyperuricemia frequently associates with respiratory diseases, patients with severe coronavirus disease 2019 (COVID-19) and severe acute respiratory syndrome (SARS) can show marked hypouricemia. Previous studies on the association of serum uric acid with risk of adverse outcomes related to COVID-19 have produced contradictory results. The precise relationship between admission serum uric acid and adverse outcomes in hospitalized patients is unknown.MethodsData of patients affected by laboratory-confirmed COVID-19 and admitted to Leishenshan Hospital were retrospectively analyzed. The primary outcome was composite and comprised events, such as intensive care unit (ICU) admission, mechanical ventilation, or mortality. Logistic regression analysis was performed to explore the association between serum concentrations of uric acid and the composite outcome, as well as each of its components. To determine the association between serum uric acid and in-hospital adverse outcomes, serum uric acid was also categorized by restricted cubic spline, and the 95% confidence interval (CI) was used to estimate odds ratios (OR).ResultsThe study cohort included 1854 patients (mean age, 58 years; 52% women). The overall mean ± SD of serum levels of uric acid was 308 ± 96 µmol/L. Among them, 95 patients were admitted to ICU, 75 patients received mechanical ventilation, and 38 died. In total, 114 patients reached composite end-points (have either ICU admission, mechanical ventilation or death) during hospitalization. Compared with a reference group with estimated baseline serum uric acid of 279-422 µmol/L, serum uric acid values ≥ 423 µmol/L were associated with an increased risk of composite outcome (OR, 2.60; 95% CI, 1.07- 6.29) and mechanical ventilation (OR, 3.01; 95% CI, 1.06- 8.51). Serum uric acid ≤ 278 µmol/L was associated with an increased risk of the composite outcome (OR, 2.07; 95% CI, 1.18- 3.65), ICU admission (OR, 2.18; 95% CI, 1.17- 4.05]), and mechanical ventilation (OR, 2.13; 95% CI, 1.06- 4.28), as assessed by multivariate analysis.ConclusionsThis study shows that the association between admission serum uric acid and composite outcome of COVID-19 patients was U-shaped. In particular, we found that compared with baseline serum uric acid levels of 279-422 µmol/L, values ≥ 423 µmol/L were associated with an increased risk of composite outcome and mechanical ventilation, whereas levels ≤ 278 µmol/L associated with increased risk of composite outcome, ICU admission and mechanical ventilation.

Serum Antioxidant Enzymes, Haematological Values and Uric Acid Concentrations in Prostatic Disease Patients: An Investigative Study

Aim: In this study, the haematology, serum antioxidant enzymes, and uric acid concentrations in prostatic disease patients attending the Nephrology Department of Abia State University Teaching Hospital, Aba were evaluated.&#x0D; Methodology: A total of one hundred and ten (110) adult males (aged 40-80 years) comprising of sixty (60) prostatic disease patients and 50 normal subjects were recruited. The prostatic disease patients comprised of 30 prostatitis, 20 Benign Prostatic Hyperplasia (BPH), and 10 prostate cancer patients. Haematological parameters, antioxidant enzyme levels, and uric acid concentration were determined on blood samples collected from the subjects between January 2017 and December 2019.&#x0D; Results: Results obtained following analysis indicated a significant fall in red blood cell count, haematocrit levels and haemoglobin concentrations in all the prostatic disease patients when compared with control subjects (p&lt;0.05) but no significant difference was observed between the values of these parameters in the three categories of patients studied (p&gt;0.05). Leukocyte and lymphocyte counts in the patients also did not significantly differ from those of the control subjects (p&gt;0.05) but platelets counts were significantly lower (p&lt;0.05). Significant elevations were observed in monocytes and granulocytes counts of prostatitis and prostate cancer patients (p&lt;0.05). Serum antioxidant enzymes activities including superoxide dismutase (SOD) and glutathione peroxidase (GPx) were lower in the prostatic disease patients than in the control (p&lt;0.05) with SOD and GPx levels being lowest in prostatitis and prostate cancer patients respectively while serum uric acid concentration was only higher than control in the prostatitis patients (p&lt;0.05).&#x0D; Conclusion: We, therefore, conclude that complications and deaths due to prostatic diseases may be due to the systemic effects of anaemia and fall in the body’s antioxidant defense line accompanying the conditions.

Association between serum uric acid and bone mineral density in patients with type 2 diabetes: A 6-year longitudinal study in China.

The relationship between serum uric acid (UA) and bone mineral density (BMD) has been proposed by several researchers. However, there has been no consensus regarding the relationships among serum UA, diabetes, and BMD. The aim of this study is to investigate the association between UA, BMD, and at least osteopenia in type 2 diabetes patients.This research was a longitudinal study performed at Xiao-Tang-Shan Hospital in Beijing. Type 2 diabetes diagnosis was consistent with the WHO standard classification. Participants with osteopenia or osteoporosis documented by dual-energy X-ray absorptiometry were defined as having “at least osteopenia.” A generalized additive model and multivariable logistic regressions were performed to explore the relationship between serum UA and at least osteopenia. Receiver operating characteristic analysis was conducted. Propensity score matching was used to verify the correctness of the cutoff point.In total, 3476 type 2 diabetes patients free of any osteopenia-related diseases were recruited in 2012 and followed up to 2018. The general proportions of patients with at least osteopenia in 2018 was 16.46% (572/3476). Serum UA was negatively associated with BMD stratified by sex, age group, and BMI level. Setting the first quartile as the reference, the risk of at least osteopenia in the fourth quartile was significant among all patients (odds ratio [OR]: 0.75; 95% confidence interval [CI]: 0.57, 0.98) and specifically in females (OR: 0.79; 95% CI: 0.43, 0.97), patients aged over 50 years (OR: 0.79; 95% CI: 0.60, 0.97) and patients with a BMI greater than 25 (OR: 0.74; 95% CI: 0.47, 0.97). The optimal cutoff point for the serum UA level to distinguish at least osteopenia in diabetic patients was 395 μmol/L.Serum UA concentration is negatively associated with the occurrence of at least osteopenia in Chinese patients with type 2 diabetes.

Fucoidan from Laminaria japonica Inhibits Expression of GLUT9 and URAT1 via PI3K/Akt, JNK and NF-κB Pathways in Uric Acid-Exposed HK-2 Cells.

This work aimed to investigate the effect of fucoidan (FPS) on urate transporters induced by uric acid (UA). The results showed that UA stimulated the expression of glucose transporter 9 (GLUT9) and urate transporter 1 (URAT1) in HK-2 cells, and FPS could reverse the effect. Moreover, UA could activate NF-κB, JNK and PI3K/Akt pathways, but both pathway inhibitors and FPS inhibited the UA-induced activation of these three pathways. These data suggested that FPS effectively inhibited the expression induction of reabsorption transporters URAT1 and GLUT9 by UA, through repressing the activation of NF-κB, JNK and PI3K/Akt signal pathways in HK-2 cells. The in vitro research findings support the in vivo results that FPS reduces serum uric acid content in hyperuricemia mice and rats through inhibiting the expression of URAT1 and GLUT9 in renal tubular epithelial cells. This study provides a theoretical basis for the application of FPS in the treatment of hyperuricemia.