Fructose-induced hyperuricemia in essential hypertension

Fiaschi, E; Baggio, Bruno; Favaro, S.; Antonello, Augusto; Camerin, E.; Todesco, S; Borsatti, A

doi:10.1016/0026-0495(77)90114-7

Cited by 16 publications

(12 citation statements)

References 13 publications

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“…It is possible that allopurinol acts more effectively under conditions in which diet is not restricted, or that its effect could be due to the prevention of leptin resistance. Second, fructose-induced hyperuricemia is maximal in the first few hours following ingestion of fructose [42,43,44] and is also dose dependent [45, 46]; thus, it is possible that the effect of UA on hyperinsulinemia and hypertriglyceridemia depend on both time of blood collection and total dose of fructose ingested.…”

Section: Discussionmentioning

confidence: 99%

Combination of Captopril and Allopurinol Retards Fructose-Induced Metabolic Syndrome

et al. 2009

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Background: Both ACE inhibitors and allopurinol have been shown to partially prevent metabolic syndrome induced by fructose. We tested the hypothesis that combined therapy might be more effective at blocking the metabolic syndrome induced with fructose. Methods: Male Sprague-Dawley rats were fed a high fructose diet with or without allopurinol, captopril, or the combination for 20 weeks. A control group received a normal diet. All groups were pair-fed to assure equivalent caloric intake. Results: Despite reduced energy intake, the fructose-fed rats developed features of metabolic syndrome including elevated blood pressure, abdominal obesity, hypertriglyceridemia, hyperuricemia and hyperinsulinemia. While both allopurinol and captopril alone tended to reduce features of the metabolic syndrome, the combined therapy was synergistic, with significant reduction in blood pressure, less accumulation of abdominal fat, an improvement in the dyslipidemia and a complete prevention of insulin resistance. Conclusion: A high fructose diet can induce metabolic syndrome even in the setting of caloric restriction. Captopril and allopurinol synergistically reduce features of the metabolic syndrome, especially hypertension, insulin resistance and dyslipidemia. Combination allopurinol and ACE inhibitor therapy might provide a superior means to prevent diabetes and cardiovascular disease.

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Section: Discussionmentioning

confidence: 99%

Combination of Captopril and Allopurinol Retards Fructose-Induced Metabolic Syndrome

et al. 2009

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“…Such has been the case when gouty patients and their progeny had a more obvious and delayed rise in uric acid than normal adults [12]. Likewise, hypertensive subjects had greater uric acid responses than normotensive subjects [13].…”

Section: Introductionmentioning

confidence: 94%

Serum Uric Acid, Inorganic Phosphorus, and Glutamic-Oxalacetic Transaminase and Blood Pressure in Carbohydrate-Sensitive Adults Consuming Three Different Levels of Sucrose

et al. 1983

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12 men and 12 women, classified as carbohydrate-sensitive on the basis of an exaggerated insulin response to a sucrose load, consumed diets containing either 5, 18, or 33 % sucrose in a crossover design. The diets simulated the average American diet and consisted of identical natural and processed foods with the exception of a patty. The patty provided the experimental levels of sucrose; the difference was made up by starch. Each level of sucrose was consumed for a 6-week period. Subject body weights were maintained. Fasting serum uric acid and inorganic phosphorus increased as the level of dietary sucrose increased. Diastolic blood pressure was significantly higher when subjects were on the 33% sucrose diet as compared to the 5 and 18 % diets. Serum glutamic-oxalacetic transaminase was not affected by diet. In tolerance tests after a sucrose load (2 g/kg body weight), the uric acid response was higher after the 18 and 33% sucrose diets than after the 5% sucrose diet. Serum inorganic phosphorus, which increased significantly with each level of dietary sucrose, decreased following the sucrose load. These results indicate that carbohydrate-sensitive individuals may be affected adversely by the level of sucrose commonly found in the Westernized diet. Since elevated serum uric acid and blood pressure have been identified as risk factors in degenerative diseases, this study suggests that carbohydrate-sensitive individuals should limit their sucrose consumption.

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“…Fructokinase has no negative feedback system, and adenosine triphosphate is used as a source of phosphorylation [26,27] . This results in intracellular phosphate depletion and the rapid generation of uric acid due to activation of adenosine monophosphate deaminase [2,26,28] . Serum uric acid increases rapidly after ingestion of fructose, resulting in increments as high as 2 mg/dl within 1 h [28] .…”

Section: Uric Acid Metabolism and Development Of Hyperuricemia With Amentioning

confidence: 99%

“…Serum uric acid increases rapidly after ingestion of fructose, resulting in increments as high as 2 mg/dl within 1 h [28] . The induction of the fructokinase enzyme by fructose in the liver provides a feed-forward mechanism for continued production of uric acid in the setting of high-fructose Western diet consumption [2,26,28] .…”

Section: Uric Acid Metabolism and Development Of Hyperuricemia With Amentioning

confidence: 99%

Uric Acid - Key Ingredient in the Recipe for Cardiorenal Metabolic Syndrome

Malhotra²,

et al. 2013

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Elevated serum uric acid levels are a frequent finding in persons with obesity, hypertension, cardiovascular and kidney disease as well as in those with the cardiorenal metabolic syndrome (CRS). The increased consumption of a fructose-rich Western diet has contributed to the increasing incidence of the CRS, obesity and diabetes especially in industrialized populations. There is also increasing evidence that supports a causal role of high dietary fructose driving elevations in uric acid in association with the CRS. Animal and epidemiological studies support the notion that elevated serum uric acid levels play an important role in promoting insulin resistance and hypertension and suggest potential pathophysiological mechanisms that contribute to the development of the CRS and associated cardiovascular disease and chronic kidney disease. To this point, elevated serum levels of uric acid appear to contribute to impaired nitric oxide production/endothelial dysfunction, increased vascular stiffness, inappropriate activation of the renin-angiotensin-aldosterone system, enhanced oxidative stress, and maladaptive immune and inflammatory responses. These abnormalities, in turn, promote vascular, cardiac and renal fibrosis as well as associated functional abnormalities. Small clinical trials have suggested that uric acid-lowering therapies may be beneficial in such patients; however, a consensus on the treatment of asymptomatic hyperuricemia is lacking. Larger randomized controlled trials need to be performed in order to critically evaluate the beneficial effect of lowering serum uric acid in patients with the CRS and those with diabetes and/or hypertension.

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Fructose-induced hyperuricemia in essential hypertension

Cited by 16 publications

References 13 publications

Combination of Captopril and Allopurinol Retards Fructose-Induced Metabolic Syndrome

Combination of Captopril and Allopurinol Retards Fructose-Induced Metabolic Syndrome

Serum Uric Acid, Inorganic Phosphorus, and Glutamic-Oxalacetic Transaminase and Blood Pressure in Carbohydrate-Sensitive Adults Consuming Three Different Levels of Sucrose

Uric Acid - Key Ingredient in the Recipe for Cardiorenal Metabolic Syndrome

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