Effect of norepinephrine on the urinary excretion of purine bases and oxypurinol

Yamamoto, Tetsuya; Moriwaki, Yuji; Takahashi, Sumio; Tsutsumi, Zenta; Hada, Toshikazu

doi:10.1053/meta.2001.26709

Cited by 38 publications

(36 citation statements)

References 15 publications

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“…Serum triglycerides and n-6 PUFAs (measured from red blood cell membranes) predict approximately one-third of the variance in SUA in healthy volunteers [51]. There is also evidence that NE exerts a modulatory effect on SUA, as administration of NE to healthy volunteers decreased SUA levels in urine [52]. In schizophrenics, evidence suggests that SUA is decreased at baseline compared to healthy controls, and that haloperidol (a dopaminergic antipsychotic) raises SUA levels in schizophrenics [53].…”

Section: Endogenous Antioxidants Correlated With Cretive Ability Are mentioning

confidence: 99%

Psychoses and creativity: is the missing link a biological mechanism related to phospholipids turnover?

Folley

Doop

Park

2003

Prostaglandins, Leukotrienes and Essential Fatty Acids

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Recent evidence suggests that genetic and biochemical factors associated with psychoses may also provide an increased propensity to think creatively. The evolutionary theories linking brain growth and diet to the appearance of creative endeavors have been made recently, but they lack a direct link to research on the biological correlates of divergent and creative thought. Expanding upon Horrobin's theory that changes in brain size and in neural microconnectivity came about as a result of changes in dietary fat and phospholipid incorporation of highly unsaturated fatty acids, we propose a theory relating phospholipase A 2 (PLA 2 ) activity to the neuromodulatory effects of the noradrenergic system. This theory offers probable links between attention, divergent thinking, and arousal through a mechanism that emphasizes optimal individual functioning of the PLA 2 and NE systems as they interact with structural and biochemical states of the brain. We hope that this theory will stimulate new research in the neural basis of creativity and its connection to psychoses.

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Section: Endogenous Antioxidants Correlated With Cretive Ability Are mentioning

confidence: 99%

Psychoses and creativity: is the missing link a biological mechanism related to phospholipids turnover?

Folley

Doop

Park

2003

Prostaglandins, Leukotrienes and Essential Fatty Acids

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“…Recently it has been reported that fenofibrate, one of the fibrates, has the effects that are observed in the fibrate class agents and the anti-hyperuricemic effect (14)(15)(16). Some authors report that the anti-hyperuricemic effect of fenofibrate comes from its uricosuric action (17). There are several reports on the anti-hyperuricemic effect of fenofibrate as mentioned above, and the reports are focused on the hyperuricemic patients or healthy volunteers.…”

Section: Introductionmentioning

confidence: 99%

Effect of Fenofibrate on Uric Acid Metabolism in Japanese Hyperlipidemic Patients

Noguchi

Tatsuno

Suyama

et al. 2004

JAT

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Forty Type IIb or IV hyperlipidemic patients (serum triglyceride concentrations were higher than 150 mg/dl) were treated with fenofibrate (300 mg/day) for 12 weeks. Lipid profile and uric acid metabolism were evaluated before and after the treatment; the serum concentrations of total cholesterol and triglyceride respectively decreased from 224 ± ± ± ± ± 41.9 mg/dl to 199 ± ± ± ± ± 35.2 mg/dl and from 205 ± ± ± ± ± 71.7 mg/dl to 134 ± ± ± ± ± 67.5 mg/dl (p < 0.001). The uric acid concentrations in the serum also significantly decreased from 7.0 ± ± ± ± ± 1.58 mg/dl to 5.2 ± ± ± ± ± 1.57 mg/dl (p < 0.001). Fenofibrate treatment did not cause any change in the serum xanthine and hypoxanthine concentrations. Instead the urinary concentrations of uric acid decreased from 7.0 ± ± ± ± ± 1.58 mg/dl to 5.2 ± ± ± ± ± 1.57 mg/dl (p < 0.01), while the clearance ratio of uric acid and creatinin increased from 6.1 ± ± ± ± ± 2.56 to 9.9 ± ± ± ± ± 3.87 (p = 0.02) by the fenofibrate treatment. Fenofibrate decreases uric acid concentrations in the serum not as a result of inhibition of uric acid production but by increasing the urinary excretion of uric acid. J Atheroscler Thromb, 2004; 11: 335-340.

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“…In hyperlipidemic patients, fenofibrate (300 mg/day) for 12 weeks decreased serum uric acid concentration by 36% and increased fractional uric acid clearance by 62% [62]. Three days' administration of fenofibrate 450 mg increased fractional clearance of uric acid, compared to baseline value, while the plasma concentration decreased in normal subjects [63]. Mechanism by which fenofibrate decreases serum uric acid levels by increasing its urinary excretion is considered to be through the inhibition of URAT1 by fenofibric acid, major metabolite of fenofibrate [64].…”

Section: Fenofibratementioning

confidence: 94%

Effects on Uric Acid Metabolism of the Drugs except the Antihyperuricemics

Moriwaki

2014

J Bioequiv Availab

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Effect of norepinephrine on the urinary excretion of purine bases and oxypurinol

Cited by 38 publications

References 15 publications

Psychoses and creativity: is the missing link a biological mechanism related to phospholipids turnover?

Psychoses and creativity: is the missing link a biological mechanism related to phospholipids turnover?

Effect of Fenofibrate on Uric Acid Metabolism in Japanese Hyperlipidemic Patients

Effects on Uric Acid Metabolism of the Drugs except the Antihyperuricemics

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