Reducing Purine Absorption through Intestinal Probiotics

2023-05-12

Hyperuricemia and gout are metabolic diseases characterized with high serum urate and impact human health significantly. In recent years, gout prevalence has risen due to changes in diet, rendering an important public health condition of worldwide concern. The global gout prevalence ranges from 0.6% to 10%. Urate is a product of purine metabolism in human. Studies have shown that about 70% and 30% urate is excreted through the kidney and gastrointestinal tract (GIT), respectively. High levels of serum urate are caused by the lack uricase enzyme that converts urate into a water-soluble and readily eliminated allantoin. 

 

Probiotics synthesize nutritional and functional metabolites to human, including vitamins, free fatty acid, γ-aminobutyric acid (GABA) and antioxidants that have vital metabolic functions. Some of the probiotics show their unique enzymatic activity to hydrolyze purines. Also, some probiotics were reported to have uricase activity that hydrolyses urate into allantoin. Accordingly, urate excretion via the GIT is made possible by urate transporter and intestinal microbiota activity. 

 

For patients with hyperuricemia, gout, metabolic syndromes and chronic kidney disease, excretion of urate relies on gut microbiota. However, imbalances of intestinal microbiota are the risk factor for increased hyperuricemia and gout possibly with reduced urate excretion. Some probiotics may produce uricase to hydrolyses urate into soluble allantoin, which is readily excreted in urine. Therefore, the intestinal microbiota can be considered as important determinants of serum urate, since they directly take part in purine catabolism and urate excretion.

 

It is advisable when targeting hyperuricemia and gout to use probiotic strains that show purine degrading characteristics because not all probiotics can utilize purines, lower serum urate, and alleviate gout. Studies showed that, probiotics mainly Bifidobacterium and Lactobacillus strains reduce urate levels as induced by the intake of the high purine diet and intraperitoneal injection of potassium oxonate. García-Arroyo et al. reported reduced urate secretion and intrarenal accumulation of urate in rats that were fed with probiotics formulated diet containing Lactobacillus acidophilus and Lactobacillus rhamnosus strains and a prebiotic xylooligosaccharides (XOS). In addition, the human studies showed that yogurt treated with Lactobacillus gasseri reduced serum urate in hyperuricemia and gout patients. Lactobacillus acidophilus and L. fermentum strains isolated from Chinese sourdough were also shown to lower serum urate. Likewise, Lactobacillus gasseri OLL2959 and Lactobacillus oris OLL2779 were shown to decompose purines and are used to treat or prevent hyperuricemia and gout. 

 

Treatment of gout with administration of purine degrading probiotics is the novel approach and demonstrates some advantages, although most of the reported data come from animal models or in vitro experiments. Nevertheless, if proved effective will have significant impact on the prevention of gout, metabolic syndrome, and comorbidities before they occur instead of only relying on drugs to treat the same. In comparison with current gout drugs, purine degrading probiotics lower serum urate via tuning functions of the gastrointestinal tract and may thus have less side effects, in addition to convenience of administration as a food or dietary supplement. Therefore, probiotics with the capacity of degrading purines are promising dietary interventions for prevention and management of hyperuricemia and gout.

 

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