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Glycine suppresses kidney calcium oxalate crystal depositions via regulating urinary excretions of oxalate and citrate
Author(s) -
Lan Yu,
Zhu Wei,
Duan Xiaolu,
Deng Tuo,
Li Shujue,
Liu Yang,
Yang Zhou,
Wen Yaoan,
Luo Lianming,
Zhao Shankun,
Wang Jiamin,
Zhao Zhijian,
Wu Wenqi,
Zeng Guohua
Publication year - 2021
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.30370
Subject(s) - calcium oxalate , oxalate , kidney stones , glycine , urine , kidney , chemistry , citric acid , in vivo , calcium , urinary system , biochemistry , medicine , biology , amino acid , endocrinology , inorganic chemistry , microbiology and biotechnology , organic chemistry
An abnormal urine composition is a key reason for kidney stone formation, but little is known about the roles of small metabolites in the urine during kidney stone formation. Here, we found urine glycine in patients with kidney calcium oxalate (CaOx) stone was significantly lower than that in healthy people via 1 H NMR spectra detection, and investigated the role and underlying mechanism of glycine in the regulation of CaOx stone formation. Our results showed that glycine could significantly attenuate ethylene glycol‐induced CaOx crystal depositions in rat kidney via decreasing urine oxalate and increasing urine citrate. Mechanism studies revealed that glycine could decrease urine oxalate through downregulating Slc26a6 expression, whereas increase urine citrate via inhibiting Nadc1 expression. Moreover, glycine decreased the protein expression of both Slc26a6 and Nadc1 via increasing the expression of miRNA‐411‐3p, which directly bound to the 3′‐untranslated regions of Slc26a6 and Nadc1 messenger RNAs, in vitro and in vivo. Together, our results revealed a novel role of glycine in the regulation of kidney CaOx crystal formation and provided a potential target for the treatment of kidney CaOx stone.