Intestinal transport of an obdurate anion: oxalate

Hatch, Marguerite; Freel, Robert W.

doi:10.1007/s00240-004-0445-3

Cited by 102 publications

(99 citation statements)

References 170 publications

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“…The fi rst peak of oxalate absorption could not be recorded in patients with a gastrectomy (12,13,93). Due to the tight epithelium, oxalate transport in the stomach is most likely transcellular (93). Immunocytochemical fi ndings of the presence of an oxalate transporter, sulfate anion (SO 4 2-) transporter Sat-1 (Slc26a1), in the oxyntic cells of the rat stomachs support claims in favour of this type of transport.…”

Section: Oxalate-handling Transporters and Their Role In Hyperoxalurimentioning

confidence: 93%

“…A few studies have shown that the stomach could be an important locus of oxalate absorption. The fi rst peak of oxalate absorption could not be recorded in patients with a gastrectomy (12,13,93). Due to the tight epithelium, oxalate transport in the stomach is most likely transcellular (93).…”

Section: Oxalate-handling Transporters and Their Role In Hyperoxalurimentioning

confidence: 96%

“…The Slc26 family of multifunctional anion exchanger proteins is believed to handle oxalate in mammalian organs (92)(93)(94)(95)) and a few specific members of this family may play a key role in the aetiology of hyperoxaluria and oxalate urolithiasis. Three organs, the intestine as an absorbing organ, liver as a metabolic organ, and kidneys as the main secretory organ, are major players in handling oxalate in the organism.…”

Section: Oxalate-handling Transporters and Their Role In Hyperoxalurimentioning

confidence: 99%

“…Similar results were obtained by applying Ang II to cultured colonic cells. Furthermore, in a rat model of CRF, oxalate excretion in the colon could be reverted by administering the AT1 receptor antagonist losartan (93,180). However, this effect was not oxalate specifi c and affected the traffi cking of several ion species, such as K + , Cl -, and urate across the colonic membranes (181).…”

Section: +mentioning

confidence: 99%

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Oxalate: From the Environment to Kidney Stones

Brzica

Breljak

Burckhardt

et al. 2013

Archives of Industrial Hygiene and Toxicology

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Oxalate urolithiasis (nephrolithiasis) is the most frequent type of kidney stone disease. Epidemiological research has shown that urolithiasis is approximately twice as common in men as in women, but the underlying mechanism of this sex-related prevalence is unclear. Oxalate in the organism partially originate from food (exogenous oxalate) and largely as a metabolic end-product from numerous precursors generated mainly in the liver (endogenous oxalate). Oxalate concentrations in plasma and urine can be modifi ed by various foodstuffs, which can interact in positively or negatively by affecting oxalate absorption, excretion, and/or its metabolic pathways. Oxalate is mostly removed from blood by kidneys and partially via bile and intestinal excretion. In the kidneys, after reaching certain conditions, such as high tubular concentration and damaged integrity of the tubule epithelium, oxalate can precipitate and initiate the formation of stones. Recent studies have indicated the importance of the SoLute Carrier 26 (SLC26) family of membrane transporters for handling oxalate. Two members of this family [Sulfate Anion Transporter 1 (SAT-1; SLC26A1) and Chloride/Formate EXchanger (CFEX; SLC26A6)] may contribute to oxalate transport in the intestine, liver, and kidneys. Malfunction or absence of SAT-1 or CFEX has been associated with hyperoxaluria and urolithiasis. However, numerous questions regarding their roles in oxalate transport in the respective organs and male-prevalent urolithiasis, as well as the role of sex hormones in the expression of these transporters at the level of mRNA and protein, still remain to be answered.

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Section: Oxalate-handling Transporters and Their Role In Hyperoxalurimentioning

confidence: 93%

Section: Oxalate-handling Transporters and Their Role In Hyperoxalurimentioning

confidence: 96%

Section: Oxalate-handling Transporters and Their Role In Hyperoxalurimentioning

confidence: 99%

Section: +mentioning

confidence: 99%

See 2 more Smart Citations

Oxalate: From the Environment to Kidney Stones

Brzica

Breljak

Burckhardt

et al. 2013

Archives of Industrial Hygiene and Toxicology

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“…The majority of anionic oxalate is thought to be absorbed via a paracellular route ( Figure 1) (15). Apical and basolateral transporters have also been demonstrated to have oxalate-transporting activity in vitro.…”

Section: Oxalate Biologymentioning

confidence: 99%

Probiotics for prevention of urinary stones

Lieske

2017

Ann. Transl. Med.

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Background: Urinary supersaturation is one key determinant of calcium oxalate (CaOx) urinary stone formation, and urinary excretions of oxalate and citrate are two key determinants. Each is influenced by gastrointestinal processes.Methods: Open label and randomized placebo studies have examined the effect of oral probiotic preparations on urinary supersaturation and oxalate excretion. Cross sectional studies in humans have studied the association of Oxalobacter formigenes colonization status and urinary oxalate excretion and prevalence of urinary stones. The intestinal microbiome of representative animals adapted to a high oxalate diet has been defined. Results:The fecal content of O. formigenes, the best studied oxalate-degrader, varies depending on stone status.However, trials with probiotics designed to degrade oxalate including those containing O. formigenes, Lactobacillus, and/or Bifidobacterium spp., have been disappointing. Multiple intestinal segments of animals on a high oxalate diet contains diverse communities of microorganisms that can function together to degrade and detoxify a large oxalate load.Conclusions: Although the intestinal microbiome seems likely to play a role to modify gastrointestinal absorption of lithogenic substances and hence urinary stone risk, whether we can develop tools to manipulate it and decrease this kidney stone risk remains to be determined.

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