To elucidate the mechanism of exercise-induced prolonged hyperuricemia, post-exercise changes in purine metabolites in plasma and plantaris muscle were examined in rats. Rats were divided into three groups including a resting control group with allopurinol (n=24) and without allopurinol (n=5), and an exercise group with allopurinol (n=48). The levels of purine metabolites were assayed by HPLC in eight or four animals each at 5,30,60,120,180, and 300 min after exhaustive exercise on the treadmill or rest. Plasma uric acid was suppressed by allopurinol both in exercise and resting control groups. Plasma inosine and hypoxanthine in the exercise group were increased between 5 and 30 min. Plasma xanthine was also increased from 5 to 180 min. Although ATP in plantaris muscle did not change at 5 min, inosine monophosphate showed an tendency to increase. Muscle inosine and hypoxanthine were increased at 5 min. Muscle hypoxanthine recovered slowly compared to inosine and the level was elevated even at 120 min. These changes of plasma and muscle purine metabolites suggest that hypoxanthineis continuously produced in fast-twitch muscles and then released from muscle to blood after exhaustive exercise, causing exercise-induced prolonged hyperuricemia.
Subjects in this study included long distance runner ( 6 men and 10 women) selected from members of a track and field club. Urine was collected two hours after the lasting voiding (immediatery after an early morning trainig session of 5 to 10km or before noon on days without training)to compare the dynamics of uric acid, hypoxanthine, and xanthine. The results are listed below: 1) The serum uric acid level among young adult long distance runners was significancy higher in men than in women. A relatively low uric acid and creatinine clearance ratio in men compared to that of women is thought to explain this difference. 2) It was suggested that exertion imposed by long distance running caused an increase in uric acid production; but no increased in the serum uric acid level was recognized in women with high uric acid clearance rates. A significant rise in the serum uric acid level was noted among men after long distance running but none developed hyperuricemic symptoms when the serum uric acid level exceeded 7.0mg/100ml. 3) Fluctuations in the levels hypoxanthine and xanthine, two precursors of uric acid, induced by long distance running were generally similar to the changing patterns of the uric acid level. It was suggested that long distance running dose not induced continued hyperuricemia.
This study is examined serum levels of uric acid in obese children to determine the relationship to regional distribution of body fat. Subjects included 60 obese children (11 girls and 49 bodys, ranging in age from 10 to 15 years). Fat distribution was evaluated by calculating the ratio of visceral fat area to subcutaneous fat area on CT scan at the umbilical level (V/Sratio). Insulin sensitivity was assessed by Σ glucose/Σ insulin on oral glucose tolerance test. Uric acid clearance was evaluated by determining the fractional excretion of uric acid (FEUA). Serum levels of uric acid correlated positively with V/S ratios. FEUA in the group with greater visceral fat was significantly lower than that in the group with greater subcutaneous fat. FEUA correlated significantly with the magnitude of insulin sensitivity. The magnitude of insulin sensitivity correlated inversely with V/S ratios. These results suggest that the excess accumulation of visceral fat may decrease uric acid clearance resulting in the progression of hyperuricinemia in childhood obesity.
We studied the relationships of HDL-cholesterol to uric acid, other lipids and degree of obesity, and the prevalence of primary hyper-HDL-cholesterolemia (over 100mg/dl) in 1342 men and 217women participating in an annual health examination. Both male and female hypo-HDL-cholesterolemic subjects (under the mean value of controls by-2SD) had significantly higher average values of body mass index(BMI) and triglycerides. The mean serum urate levels were 6.5±0.2mg/dl(mean±SEM) in men (control,5.5±0.1mg/dl, p<0.01)and 4.8±0.3mg/dl in women (control,4.0±0.1mg/dl, p<0.05), respectively. In male hyper-HDL-cholesterolemic subjects (over the mean value of controls by+2SD), mean triglycerides levels appeared significantly lower (p<0.01), and that of female subjects had a tendency to be lower, with a mean values of 57±6mg/dl(control,73±4mg/dl). The mean serum urate levels were 3.6±0.1mg/dl in females, lower than the control values, and 5.8±0.1mg/cle in males, higher than the control levels, neither significantly. The higher serum urate level in males was attributed to the fact that 91.2% of the group were alcohol drinkers with an average daily alcohol intake of 30.4gr. Hyper-HDL-cholesterolemic subjects, whose HDL-cholesterol level was over 90mg/dl, showed a slightly lower mean values for BMI 20.7±0.7 in males(control,21.5±0.3) and significantly lower average levels for BMI 19.1±0.5 in females(control,20.9±0.3, p<0.05). However, hyper-HDL-cholesterolemic subjects as a whole did not show significantly lower values for BMI compared with controls. Correlation coefficients between the serum HDL-cholesterol level and urate were significant -0.299 in males(p<0.05) and insignificant -0.102 in females. HDL-cholesterol is closely related to obesity, so hypo-HDL-cholesterolemic subjects have higher values of BMI, triglycerides and uric acid. The prevalence of primary hyper-HDL-cholesterolemia was 0.4% in males and 1.3% in females.