Relationship of Serum Uric Acid Concentration to Metabolic Syndrome: Age and Gender Discrepancies.

2010 ◽  
pp. P1-449-P1-449
Author(s):  
WK Chiou ◽  
MH Wang ◽  
DH Huang ◽  
HT Chiu ◽  
YJ Lee ◽  
...  
2021 ◽  
Vol 2021 ◽  
pp. 1-7
Author(s):  
Anna Masajtis-Zagajewska ◽  
Jacek Majer ◽  
Michał Nowicki

Introduction. Excessive intake of fructose increases serum uric acid concentration. Hyperuricemia induces a negative effect on atherosclerosis and inflammation. Hyperuricemia is common in patients with arterial hypertension. Several antihypertensive drugs including diuretics increase serum uric acid concentration. In contrast, the angiotensin II receptor antagonist (ARB) losartan was found to lower serum uric acid though it may increase renal excretion while other ARBs showed mostly a neutral effect. In this study, effects of two AT1 receptor antagonists losartan and eprosartan on serum uric acid changes induced by oral fructose load were directly compared. Methods. The randomized, crossover, head-to-head comparative study comprised 16 ambulatory patients (mean age 64.5 ± 9.8 years). The patients fulfilled AHA/NHLBI 2005 criteria of metabolic syndrome. A daily single morning dose of each study drug (50 mg of losartan or 600 mg of eprosartan) was given during two 3-month periods in a random order separated by 2-week washout time. The oral fructose tolerance test (OFTT) was performed at baseline and after each two 3-onth treatment periods. Before and during OFTT, urine excretion of uric acid and creatinine was assessed in the first morning portion of urine. Blood samples for the measurement of serum uric acid and lipids were taken at baseline and 30, 60, and 120 minutes after oral intake of 75 g of fructose. Results. After 3-month treatment with eprosartan and losartan, both systolic and diastolic blood pressure decreased significantly and to a similar extent. After the treatment, serum uric acid and its baseline and postfructose urine excretion were unchanged. No significant changes of plasma lipids before and after OFTT were observed throughout the study. Conclusions. The study showed that in patients with hypertension and metabolic syndrome, both losartan and eprosartan have a neutral effect on fasting and postfructose load serum uric acid concentration and its urinary excretion. This trial is registered with NCT04954560.


2005 ◽  
Vol 69 (8) ◽  
pp. 928-933 ◽  
Author(s):  
Tae Woo Yoo ◽  
Ki Chul Sung ◽  
Hun Sub Shin ◽  
Byung Jin Kim ◽  
Bum Soo Kim ◽  
...  

2018 ◽  
Vol 12 (3) ◽  
pp. 325-331 ◽  
Author(s):  
Leonardo M. Porchia ◽  
M. Elba Gonzalez-Mejia ◽  
Enrique Torres-Rasgado ◽  
Guadalupe Ruiz-Vivanco ◽  
Ricardo Pérez-Fuentes

2006 ◽  
Vol 34 (01) ◽  
pp. 77-85 ◽  
Author(s):  
Guang-Liang Chen ◽  
Wei Wei ◽  
Shu-Yun Xu

In this study, we investigated the effects and mechanisms of Total Saponin of Dioscorea (TSD) on animal experimental hyperuricemia. Mouse and rat hyperuricemic models were made by orally administering yeast extract paste once a day (30 and 20 g/kg, respectively), for 7 days. Yeast would disturb normal purine metabolism by increasing xanthine oxidase (XOD) activity and generating large quantities of uric acid. This model is similar to human hyperuricemia, which is induced by high-protein diets, due to a purine and nucleic acid metabolic disturbance. Another mouse hyperuricemia model was generated by intraperitoneal injection once with uric acid 250 mg/kg or potassium oxonate 300 mg/kg. Potassium oxonate, a urate oxidase inhibitor, can raise the serum uric acid level by inhibiting the decomposition of uric acid. Likewise, injecting uric acid can also increase serum uric acid concentration. The concentration of uric acid in serum or urine was detected by the phosphotungstic acid method, and the activity of XOD was assayed by a test kit. The results showed that TSD (240, 120 and 60 mg/kg, ig) could significantly lower the level of serum uric acid in hyperuricemic mice. TSD (120 and 60 mg/kg, ig) could also lower the level of serum uric acid in hyperuricemic rats, reduce the activity of XOD in the serum and liver of hyperuricemic rats, and increase the level of urine uric acid concentration as well as 24-hour total uric acid excretion. In conclusion, TSD possesses a potent anti-hyperuricemic effect on hyperuricemic animals, and the mechanism may be relevant in accelerating the excretion and decreasing the production of uric acid.


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