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Dietary hyperoxaluria is not reduced by treatment with lactic acid bacteria

BACKGROUND: Secondary hyperoxaluria either based on increased intestinal absorption of oxalate (enteric), or high oxalate intake (dietary), is a major risk factor of calcium oxalate urolithiasis. Oxalate-degrading bacteria might have beneficial effects on urinary oxalate excretion resulting from dec...

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Autores principales: Siener, Roswitha, Bade, Diana J, Hesse, Albrecht, Hoppe, Bernd
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4029792/
https://www.ncbi.nlm.nih.gov/pubmed/24330782
http://dx.doi.org/10.1186/1479-5876-11-306
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author Siener, Roswitha
Bade, Diana J
Hesse, Albrecht
Hoppe, Bernd
author_facet Siener, Roswitha
Bade, Diana J
Hesse, Albrecht
Hoppe, Bernd
author_sort Siener, Roswitha
collection PubMed
description BACKGROUND: Secondary hyperoxaluria either based on increased intestinal absorption of oxalate (enteric), or high oxalate intake (dietary), is a major risk factor of calcium oxalate urolithiasis. Oxalate-degrading bacteria might have beneficial effects on urinary oxalate excretion resulting from decreased intestinal oxalate concentration and absorption. METHODS: Twenty healthy subjects were studied initially while consuming a diet normal in oxalate. Study participants were then placed on a controlled oxalate-rich diet for a period of 6 weeks. Starting with week 2 of the oxalate-rich diet, participants received 2.6 g/day of a lactic acid bacteria preparation for 5 weeks. Finally, subjects were examined 4 weeks after treatment while consuming again a normal-oxalate diet. Participants provided weekly 24-hour urine specimens. Analyses of blood samples were performed before and at the end of treatment. RESULTS: Urinary oxalate excretion increased significantly from 0.354 ± 0.097 at baseline to 0.542 ± 0.163 mmol/24 h under the oxalate-rich diet and remained elevated until the end of treatment, as did relative supersaturation of calcium oxalate. Plasma oxalate concentration was significantly higher after 5 weeks of treatment compared to baseline. Four weeks after treatment, urinary oxalate excretion and relative supersaturation of calcium oxalate fell to reach initial values. CONCLUSIONS: Persistent dietary hyperoxaluria and increased plasma oxalate concentration can already be induced in healthy subjects without disorders of oxalate metabolism. The study preparation neither reduced urinary oxalate excretion nor plasma oxalate concentration. The preparation may be altered to select for lactic acid bacteria strains with the highest oxalate-degrading activity.
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spelling pubmed-40297922014-05-22 Dietary hyperoxaluria is not reduced by treatment with lactic acid bacteria Siener, Roswitha Bade, Diana J Hesse, Albrecht Hoppe, Bernd J Transl Med Research BACKGROUND: Secondary hyperoxaluria either based on increased intestinal absorption of oxalate (enteric), or high oxalate intake (dietary), is a major risk factor of calcium oxalate urolithiasis. Oxalate-degrading bacteria might have beneficial effects on urinary oxalate excretion resulting from decreased intestinal oxalate concentration and absorption. METHODS: Twenty healthy subjects were studied initially while consuming a diet normal in oxalate. Study participants were then placed on a controlled oxalate-rich diet for a period of 6 weeks. Starting with week 2 of the oxalate-rich diet, participants received 2.6 g/day of a lactic acid bacteria preparation for 5 weeks. Finally, subjects were examined 4 weeks after treatment while consuming again a normal-oxalate diet. Participants provided weekly 24-hour urine specimens. Analyses of blood samples were performed before and at the end of treatment. RESULTS: Urinary oxalate excretion increased significantly from 0.354 ± 0.097 at baseline to 0.542 ± 0.163 mmol/24 h under the oxalate-rich diet and remained elevated until the end of treatment, as did relative supersaturation of calcium oxalate. Plasma oxalate concentration was significantly higher after 5 weeks of treatment compared to baseline. Four weeks after treatment, urinary oxalate excretion and relative supersaturation of calcium oxalate fell to reach initial values. CONCLUSIONS: Persistent dietary hyperoxaluria and increased plasma oxalate concentration can already be induced in healthy subjects without disorders of oxalate metabolism. The study preparation neither reduced urinary oxalate excretion nor plasma oxalate concentration. The preparation may be altered to select for lactic acid bacteria strains with the highest oxalate-degrading activity. BioMed Central 2013-12-12 /pmc/articles/PMC4029792/ /pubmed/24330782 http://dx.doi.org/10.1186/1479-5876-11-306 Text en Copyright © 2013 Siener et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research
Siener, Roswitha
Bade, Diana J
Hesse, Albrecht
Hoppe, Bernd
Dietary hyperoxaluria is not reduced by treatment with lactic acid bacteria
title Dietary hyperoxaluria is not reduced by treatment with lactic acid bacteria
title_full Dietary hyperoxaluria is not reduced by treatment with lactic acid bacteria
title_fullStr Dietary hyperoxaluria is not reduced by treatment with lactic acid bacteria
title_full_unstemmed Dietary hyperoxaluria is not reduced by treatment with lactic acid bacteria
title_short Dietary hyperoxaluria is not reduced by treatment with lactic acid bacteria
title_sort dietary hyperoxaluria is not reduced by treatment with lactic acid bacteria
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4029792/
https://www.ncbi.nlm.nih.gov/pubmed/24330782
http://dx.doi.org/10.1186/1479-5876-11-306
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