Abstract
Hyperuricemia is highly prevalent and especially common in subjects with metabolic, cardiovascular and renal diseases. In chronic kidney disease, hyperuricemia is extremely common, and uric acid (UA) excretion relies on gut uricolysis by gut microbiota. Current therapy for lowering serum UA includes drugs that may produce undesired secondary effects. Therefore, this pilot study was designed to evaluate the potential of two probiotic supplements to reduce systemic uric acid concentrations. Secondary objectives were to assess whether the hypouricemic effect related to a therapeutic benefit on the hyperuricemia-induced renal damage and hypertension. Analysis of fecal microbiota was also performed. Groups of 6 rats each were followed for 5 weeks and allocated in the following treatment groups: C = Control; HU-ND = Oxonic acid-induced hyperuricemia (HU) +regular diet; HU-P = HU+placebo; HU-F1 = HU+ probiotics formula 1 and HU-F2 = HU+ probiotics formula 2. We confirmed that oxonic acid-induced hyperuricemia produced hypertension and renal functional and structural changes, along with modest changes in the overall composition of fecal microbiota. Both probiotic-containing diets prevented HU, elevated UA urinary excretion and intrarenal UA accumulation induced by oxonic acid. The hypouricemic effect conferred by probiotic supplementation also prevented the renal changes and hypertension caused by hyperuricemia. However, probiotic treatment did not restore the fecal microbiota. In conclusion, we demonstrated for the first time the ability of probiotics containing uricolytic bacteria to lower serum uric acid in hyperuricemic animals with beneficial consequences on blood pressure and renal disease. As probiotics supplements are innocuous for human health, we recommend clinical studies to test if probiotic supplements could benefit hyperuricemic individuals.
Highlights
Hyperuricemia is often present in the population, with some studies reporting a prevalence as high as 21% in men and women [1]
In the control (C) group, PUA remained unchanged during the 5 weeks of follow-up
At the end of the study HU-F1 and HU-F2 groups had higher PUA concentrations compared to their respective baselines, still the levels were significantly lower compared to HU-ND and HU-P groups at 3 weeks with even greater differences in plasma uric acid at 5 weeks of follow-up
Summary
Hyperuricemia is often present in the population, with some studies reporting a prevalence as high as 21% in men and women [1]. Hyperuricemia is especially common in subjects with metabolic, cardiovascular and renal diseases [2,3,4]. While the presence of hyperuricemia in the absence of gout has often been described as “asymptomatic”, recent studies suggest hyperuricemia may have a contributory role in metabolic and cardiovascular diseases. Depending on the cell type, UA may cause increased proliferation (VSMC) [5, 6] or apoptosis (renal tubular cells, endothelial cells) [7, 8]. While UA is a prooxidant in the intracellular environment, uric acid may function as an anti-oxidant and has been proposed to protect the central nervous system in conditions such as Parkinson’s disease [9]
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