| Co-Investigator(Kenkyū-buntansha) |
HOKAMA Sanehiro University of the Ryukyus, Faculty of Medicine, Urology, Lecturer, 医学部, 助手 (20229157)
MOROZUMI Makoto University of the Ryukyus, Faculty of Medicine, Urology, Assistant Professor, 医学部附属病院, 講師 (60166460)
HATANO Tadashi University of the Ryukyus, Faculty of Medicine, Urology, Associate Professor, 医学部, 助教授 (10101924)
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| Research Abstract |
Calcium oxalate alone or in combination with calcium phosphate have been documented as major components of urinary calculi in Okinawa. Calcium oxalate urolithiasis is usually idiopathic, and about 1/3 is associated with hyperoxaluria and another 1/3 is associated with hypercalciuria. Urinary excretion of oxalate increases after the ingestion of oxalate-rich and fatty foods, as well as in the absence of oxalate-degrading intestinal flora. Oxalate-degrading bacteria in the human intestine are obligatory anaerobes, with Oxalobacter formigenes being reported as the first of such bacteria that are widely known to reside in the human bowel. We isolated two oxalate-degrading facultative anaerobes from humans, which were Enterococcus fecalis and Providencia rettgerii. These organisms grew under routine laboratory conditions without complex requirements, but tended to lose their oxalate-degrading activity in routine culture. We have also searched for oxalate-degrading activity in 25 probiotic supplements, including a Lactobacillus drink, but so far no such activity has been found.
We have established rat models of oxalate absorption to study the site of oxalate absorption (stomach, small intestine, or colon), and the inhibitors of absorption like calcium and magnesium. Further studies need to be done on other substances, such as fatty acids and bile acids.
Oxalate is known to be a uremic toxin, and we have shown that is mainly derived from ascorbic acid. Long-standing hyperoxalemia may cause tissue deposition of calcium oxalate. If ascorbic acid is converted into oxalate in the intestine, intestinal oxalate-degrading bacteria may promote the inhibition of oxalate absorption in patients with renal failure.
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