Butyrate production in patients with end-stage renal disease
Matty L Terpstra,1–3 Marjan J Sinnige,1,3 Floor Hugenholtz,4 Hessel Peters-Sengers,4 Ester BM Remmerswaal,1,3 Suzanne E Geerlings,2 Frederike J Bemelman11Department of Internal Medicine, Division of Nephrology, Renal Transplant Unit, Amsterdam UMC, University of Amsterdam, Amsterdam, Nethe...
Ausführliche Beschreibung
Autor*in: |
Terpstra ML [verfasserIn] Sinnige MJ [verfasserIn] Hugenholtz F [verfasserIn] Peters-Sengers H [verfasserIn] Remmerswaal EBM [verfasserIn] Geerlings SE [verfasserIn] Bemelman FJ [verfasserIn] |
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E-Artikel |
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Englisch |
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2019 |
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In: International Journal of Nephrology and Renovascular Disease - Dove Medical Press, 2009, (2019), Seite 87-101 |
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Übergeordnetes Werk: |
year:2019 ; pages:87-101 |
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DOAJ05437054X |
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520 | |a Matty L Terpstra,1–3 Marjan J Sinnige,1,3 Floor Hugenholtz,4 Hessel Peters-Sengers,4 Ester BM Remmerswaal,1,3 Suzanne E Geerlings,2 Frederike J Bemelman11Department of Internal Medicine, Division of Nephrology, Renal Transplant Unit, Amsterdam UMC, University of Amsterdam, Amsterdam, Netherlands; 2Department of Internal Medicine, Division of Infectious Diseases, Amsterdam Infection & Immunity Institute (AI&II), Amsterdam UMC, University of Amsterdam, Amsterdam, The Netherlands; 3Department of Experimental Immunology, Amsterdam Infection & Immunity Institute (AI&II), Amsterdam UMC, University of Amsterdam, Amsterdam, The Netherlands; 4Center for Experimental and Molecular Medicine, Amsterdam UMC, University of Amsterdam, Amsterdam, NetherlandsBackground: Chronic kidney disease (CKD) is associated with a decreased intestinal barrier function, causing bacterial translocation over the intestinal wall and triggering a systemic inflammatory response. Butyrate, a short-chain fatty acid produced by certain bacterial strains, is considered instrumental to keep the intestinal barrier intact. There are indications that a decreased amount of these specific bacterial species is part of the cause of the decreased intestinal barrier function in CKD. The aim of this study is (i) to determine if Dutch patients with end-stage renal disease (ESRD) have a decreased amount of butyrate-producing species and butyrate-producing capacity and (ii) whether this correlates with systemic inflammation.Methods: We used qPCR to evaluate the most abundant butyrate-producing species F. prauznitzii, E. rectale and Roseburia spp. and the BCoAT gene, which reflects the butyrogenic capacity of the intestinal microbiota. Fecal samples were collected from healthy kidney donors (n=15), preemptive renal transplant recipients (n=4) and dialysis patients (n=31). Markers of inflammation (CRP and IL-6) and intestinal permeability (D-lactate) were measured in plasma.Results: Patients with ESRD did not have a significantly decreased amount F. prauznitzii, E. rectale and Roseburia spp. or the BCoAT gene. Neither was there a significant correlation with CRP, IL-6 or D-lactate. On the individual level, there were some patients with decreased BCoAT levels and increased levels of CRP, IL-6 and D-lactate.Conclusions: Patients with ESRD do not have a decreased amount of the most abundant butyrate-producing species nor a decreased butyrate-producing capacity.Keywords: renal failure, intestinal barrier function, butyrate, intestinal microbiota, inflammation | ||
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(DE-627)DOAJ05437054X (DE-599)DOAJcf2d53d55fee4d198916ddcd0a03fbda DE-627 ger DE-627 rakwb eng RC870-923 Terpstra ML verfasserin aut Butyrate production in patients with end-stage renal disease 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Matty L Terpstra,1–3 Marjan J Sinnige,1,3 Floor Hugenholtz,4 Hessel Peters-Sengers,4 Ester BM Remmerswaal,1,3 Suzanne E Geerlings,2 Frederike J Bemelman11Department of Internal Medicine, Division of Nephrology, Renal Transplant Unit, Amsterdam UMC, University of Amsterdam, Amsterdam, Netherlands; 2Department of Internal Medicine, Division of Infectious Diseases, Amsterdam Infection & Immunity Institute (AI&II), Amsterdam UMC, University of Amsterdam, Amsterdam, The Netherlands; 3Department of Experimental Immunology, Amsterdam Infection & Immunity Institute (AI&II), Amsterdam UMC, University of Amsterdam, Amsterdam, The Netherlands; 4Center for Experimental and Molecular Medicine, Amsterdam UMC, University of Amsterdam, Amsterdam, NetherlandsBackground: Chronic kidney disease (CKD) is associated with a decreased intestinal barrier function, causing bacterial translocation over the intestinal wall and triggering a systemic inflammatory response. Butyrate, a short-chain fatty acid produced by certain bacterial strains, is considered instrumental to keep the intestinal barrier intact. There are indications that a decreased amount of these specific bacterial species is part of the cause of the decreased intestinal barrier function in CKD. The aim of this study is (i) to determine if Dutch patients with end-stage renal disease (ESRD) have a decreased amount of butyrate-producing species and butyrate-producing capacity and (ii) whether this correlates with systemic inflammation.Methods: We used qPCR to evaluate the most abundant butyrate-producing species F. prauznitzii, E. rectale and Roseburia spp. and the BCoAT gene, which reflects the butyrogenic capacity of the intestinal microbiota. Fecal samples were collected from healthy kidney donors (n=15), preemptive renal transplant recipients (n=4) and dialysis patients (n=31). Markers of inflammation (CRP and IL-6) and intestinal permeability (D-lactate) were measured in plasma.Results: Patients with ESRD did not have a significantly decreased amount F. prauznitzii, E. rectale and Roseburia spp. or the BCoAT gene. Neither was there a significant correlation with CRP, IL-6 or D-lactate. On the individual level, there were some patients with decreased BCoAT levels and increased levels of CRP, IL-6 and D-lactate.Conclusions: Patients with ESRD do not have a decreased amount of the most abundant butyrate-producing species nor a decreased butyrate-producing capacity.Keywords: renal failure, intestinal barrier function, butyrate, intestinal microbiota, inflammation renal failure intestinal barrier function butyrate intestinal microbiota inflammation Diseases of the genitourinary system. Urology Sinnige MJ verfasserin aut Hugenholtz F verfasserin aut Peters-Sengers H verfasserin aut Remmerswaal EBM verfasserin aut Geerlings SE verfasserin aut Bemelman FJ verfasserin aut In International Journal of Nephrology and Renovascular Disease Dove Medical Press, 2009 (2019), Seite 87-101 (DE-627)606031928 (DE-600)2508160-3 11787058 nnns year:2019 pages:87-101 https://doaj.org/article/cf2d53d55fee4d198916ddcd0a03fbda kostenfrei https://www.dovepress.com/butyrate-production-in-patients-with-end-stage-renal-disease-peer-reviewed-article-IJNRD kostenfrei https://doaj.org/toc/1178-7058 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 2019 87-101 |
spelling |
(DE-627)DOAJ05437054X (DE-599)DOAJcf2d53d55fee4d198916ddcd0a03fbda DE-627 ger DE-627 rakwb eng RC870-923 Terpstra ML verfasserin aut Butyrate production in patients with end-stage renal disease 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Matty L Terpstra,1–3 Marjan J Sinnige,1,3 Floor Hugenholtz,4 Hessel Peters-Sengers,4 Ester BM Remmerswaal,1,3 Suzanne E Geerlings,2 Frederike J Bemelman11Department of Internal Medicine, Division of Nephrology, Renal Transplant Unit, Amsterdam UMC, University of Amsterdam, Amsterdam, Netherlands; 2Department of Internal Medicine, Division of Infectious Diseases, Amsterdam Infection & Immunity Institute (AI&II), Amsterdam UMC, University of Amsterdam, Amsterdam, The Netherlands; 3Department of Experimental Immunology, Amsterdam Infection & Immunity Institute (AI&II), Amsterdam UMC, University of Amsterdam, Amsterdam, The Netherlands; 4Center for Experimental and Molecular Medicine, Amsterdam UMC, University of Amsterdam, Amsterdam, NetherlandsBackground: Chronic kidney disease (CKD) is associated with a decreased intestinal barrier function, causing bacterial translocation over the intestinal wall and triggering a systemic inflammatory response. Butyrate, a short-chain fatty acid produced by certain bacterial strains, is considered instrumental to keep the intestinal barrier intact. There are indications that a decreased amount of these specific bacterial species is part of the cause of the decreased intestinal barrier function in CKD. The aim of this study is (i) to determine if Dutch patients with end-stage renal disease (ESRD) have a decreased amount of butyrate-producing species and butyrate-producing capacity and (ii) whether this correlates with systemic inflammation.Methods: We used qPCR to evaluate the most abundant butyrate-producing species F. prauznitzii, E. rectale and Roseburia spp. and the BCoAT gene, which reflects the butyrogenic capacity of the intestinal microbiota. Fecal samples were collected from healthy kidney donors (n=15), preemptive renal transplant recipients (n=4) and dialysis patients (n=31). Markers of inflammation (CRP and IL-6) and intestinal permeability (D-lactate) were measured in plasma.Results: Patients with ESRD did not have a significantly decreased amount F. prauznitzii, E. rectale and Roseburia spp. or the BCoAT gene. Neither was there a significant correlation with CRP, IL-6 or D-lactate. On the individual level, there were some patients with decreased BCoAT levels and increased levels of CRP, IL-6 and D-lactate.Conclusions: Patients with ESRD do not have a decreased amount of the most abundant butyrate-producing species nor a decreased butyrate-producing capacity.Keywords: renal failure, intestinal barrier function, butyrate, intestinal microbiota, inflammation renal failure intestinal barrier function butyrate intestinal microbiota inflammation Diseases of the genitourinary system. Urology Sinnige MJ verfasserin aut Hugenholtz F verfasserin aut Peters-Sengers H verfasserin aut Remmerswaal EBM verfasserin aut Geerlings SE verfasserin aut Bemelman FJ verfasserin aut In International Journal of Nephrology and Renovascular Disease Dove Medical Press, 2009 (2019), Seite 87-101 (DE-627)606031928 (DE-600)2508160-3 11787058 nnns year:2019 pages:87-101 https://doaj.org/article/cf2d53d55fee4d198916ddcd0a03fbda kostenfrei https://www.dovepress.com/butyrate-production-in-patients-with-end-stage-renal-disease-peer-reviewed-article-IJNRD kostenfrei https://doaj.org/toc/1178-7058 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 2019 87-101 |
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(DE-627)DOAJ05437054X (DE-599)DOAJcf2d53d55fee4d198916ddcd0a03fbda DE-627 ger DE-627 rakwb eng RC870-923 Terpstra ML verfasserin aut Butyrate production in patients with end-stage renal disease 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Matty L Terpstra,1–3 Marjan J Sinnige,1,3 Floor Hugenholtz,4 Hessel Peters-Sengers,4 Ester BM Remmerswaal,1,3 Suzanne E Geerlings,2 Frederike J Bemelman11Department of Internal Medicine, Division of Nephrology, Renal Transplant Unit, Amsterdam UMC, University of Amsterdam, Amsterdam, Netherlands; 2Department of Internal Medicine, Division of Infectious Diseases, Amsterdam Infection & Immunity Institute (AI&II), Amsterdam UMC, University of Amsterdam, Amsterdam, The Netherlands; 3Department of Experimental Immunology, Amsterdam Infection & Immunity Institute (AI&II), Amsterdam UMC, University of Amsterdam, Amsterdam, The Netherlands; 4Center for Experimental and Molecular Medicine, Amsterdam UMC, University of Amsterdam, Amsterdam, NetherlandsBackground: Chronic kidney disease (CKD) is associated with a decreased intestinal barrier function, causing bacterial translocation over the intestinal wall and triggering a systemic inflammatory response. Butyrate, a short-chain fatty acid produced by certain bacterial strains, is considered instrumental to keep the intestinal barrier intact. There are indications that a decreased amount of these specific bacterial species is part of the cause of the decreased intestinal barrier function in CKD. The aim of this study is (i) to determine if Dutch patients with end-stage renal disease (ESRD) have a decreased amount of butyrate-producing species and butyrate-producing capacity and (ii) whether this correlates with systemic inflammation.Methods: We used qPCR to evaluate the most abundant butyrate-producing species F. prauznitzii, E. rectale and Roseburia spp. and the BCoAT gene, which reflects the butyrogenic capacity of the intestinal microbiota. Fecal samples were collected from healthy kidney donors (n=15), preemptive renal transplant recipients (n=4) and dialysis patients (n=31). Markers of inflammation (CRP and IL-6) and intestinal permeability (D-lactate) were measured in plasma.Results: Patients with ESRD did not have a significantly decreased amount F. prauznitzii, E. rectale and Roseburia spp. or the BCoAT gene. Neither was there a significant correlation with CRP, IL-6 or D-lactate. On the individual level, there were some patients with decreased BCoAT levels and increased levels of CRP, IL-6 and D-lactate.Conclusions: Patients with ESRD do not have a decreased amount of the most abundant butyrate-producing species nor a decreased butyrate-producing capacity.Keywords: renal failure, intestinal barrier function, butyrate, intestinal microbiota, inflammation renal failure intestinal barrier function butyrate intestinal microbiota inflammation Diseases of the genitourinary system. Urology Sinnige MJ verfasserin aut Hugenholtz F verfasserin aut Peters-Sengers H verfasserin aut Remmerswaal EBM verfasserin aut Geerlings SE verfasserin aut Bemelman FJ verfasserin aut In International Journal of Nephrology and Renovascular Disease Dove Medical Press, 2009 (2019), Seite 87-101 (DE-627)606031928 (DE-600)2508160-3 11787058 nnns year:2019 pages:87-101 https://doaj.org/article/cf2d53d55fee4d198916ddcd0a03fbda kostenfrei https://www.dovepress.com/butyrate-production-in-patients-with-end-stage-renal-disease-peer-reviewed-article-IJNRD kostenfrei https://doaj.org/toc/1178-7058 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 2019 87-101 |
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(DE-627)DOAJ05437054X (DE-599)DOAJcf2d53d55fee4d198916ddcd0a03fbda DE-627 ger DE-627 rakwb eng RC870-923 Terpstra ML verfasserin aut Butyrate production in patients with end-stage renal disease 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Matty L Terpstra,1–3 Marjan J Sinnige,1,3 Floor Hugenholtz,4 Hessel Peters-Sengers,4 Ester BM Remmerswaal,1,3 Suzanne E Geerlings,2 Frederike J Bemelman11Department of Internal Medicine, Division of Nephrology, Renal Transplant Unit, Amsterdam UMC, University of Amsterdam, Amsterdam, Netherlands; 2Department of Internal Medicine, Division of Infectious Diseases, Amsterdam Infection & Immunity Institute (AI&II), Amsterdam UMC, University of Amsterdam, Amsterdam, The Netherlands; 3Department of Experimental Immunology, Amsterdam Infection & Immunity Institute (AI&II), Amsterdam UMC, University of Amsterdam, Amsterdam, The Netherlands; 4Center for Experimental and Molecular Medicine, Amsterdam UMC, University of Amsterdam, Amsterdam, NetherlandsBackground: Chronic kidney disease (CKD) is associated with a decreased intestinal barrier function, causing bacterial translocation over the intestinal wall and triggering a systemic inflammatory response. Butyrate, a short-chain fatty acid produced by certain bacterial strains, is considered instrumental to keep the intestinal barrier intact. There are indications that a decreased amount of these specific bacterial species is part of the cause of the decreased intestinal barrier function in CKD. The aim of this study is (i) to determine if Dutch patients with end-stage renal disease (ESRD) have a decreased amount of butyrate-producing species and butyrate-producing capacity and (ii) whether this correlates with systemic inflammation.Methods: We used qPCR to evaluate the most abundant butyrate-producing species F. prauznitzii, E. rectale and Roseburia spp. and the BCoAT gene, which reflects the butyrogenic capacity of the intestinal microbiota. Fecal samples were collected from healthy kidney donors (n=15), preemptive renal transplant recipients (n=4) and dialysis patients (n=31). Markers of inflammation (CRP and IL-6) and intestinal permeability (D-lactate) were measured in plasma.Results: Patients with ESRD did not have a significantly decreased amount F. prauznitzii, E. rectale and Roseburia spp. or the BCoAT gene. Neither was there a significant correlation with CRP, IL-6 or D-lactate. On the individual level, there were some patients with decreased BCoAT levels and increased levels of CRP, IL-6 and D-lactate.Conclusions: Patients with ESRD do not have a decreased amount of the most abundant butyrate-producing species nor a decreased butyrate-producing capacity.Keywords: renal failure, intestinal barrier function, butyrate, intestinal microbiota, inflammation renal failure intestinal barrier function butyrate intestinal microbiota inflammation Diseases of the genitourinary system. Urology Sinnige MJ verfasserin aut Hugenholtz F verfasserin aut Peters-Sengers H verfasserin aut Remmerswaal EBM verfasserin aut Geerlings SE verfasserin aut Bemelman FJ verfasserin aut In International Journal of Nephrology and Renovascular Disease Dove Medical Press, 2009 (2019), Seite 87-101 (DE-627)606031928 (DE-600)2508160-3 11787058 nnns year:2019 pages:87-101 https://doaj.org/article/cf2d53d55fee4d198916ddcd0a03fbda kostenfrei https://www.dovepress.com/butyrate-production-in-patients-with-end-stage-renal-disease-peer-reviewed-article-IJNRD kostenfrei https://doaj.org/toc/1178-7058 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 2019 87-101 |
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(DE-627)DOAJ05437054X (DE-599)DOAJcf2d53d55fee4d198916ddcd0a03fbda DE-627 ger DE-627 rakwb eng RC870-923 Terpstra ML verfasserin aut Butyrate production in patients with end-stage renal disease 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Matty L Terpstra,1–3 Marjan J Sinnige,1,3 Floor Hugenholtz,4 Hessel Peters-Sengers,4 Ester BM Remmerswaal,1,3 Suzanne E Geerlings,2 Frederike J Bemelman11Department of Internal Medicine, Division of Nephrology, Renal Transplant Unit, Amsterdam UMC, University of Amsterdam, Amsterdam, Netherlands; 2Department of Internal Medicine, Division of Infectious Diseases, Amsterdam Infection & Immunity Institute (AI&II), Amsterdam UMC, University of Amsterdam, Amsterdam, The Netherlands; 3Department of Experimental Immunology, Amsterdam Infection & Immunity Institute (AI&II), Amsterdam UMC, University of Amsterdam, Amsterdam, The Netherlands; 4Center for Experimental and Molecular Medicine, Amsterdam UMC, University of Amsterdam, Amsterdam, NetherlandsBackground: Chronic kidney disease (CKD) is associated with a decreased intestinal barrier function, causing bacterial translocation over the intestinal wall and triggering a systemic inflammatory response. Butyrate, a short-chain fatty acid produced by certain bacterial strains, is considered instrumental to keep the intestinal barrier intact. There are indications that a decreased amount of these specific bacterial species is part of the cause of the decreased intestinal barrier function in CKD. The aim of this study is (i) to determine if Dutch patients with end-stage renal disease (ESRD) have a decreased amount of butyrate-producing species and butyrate-producing capacity and (ii) whether this correlates with systemic inflammation.Methods: We used qPCR to evaluate the most abundant butyrate-producing species F. prauznitzii, E. rectale and Roseburia spp. and the BCoAT gene, which reflects the butyrogenic capacity of the intestinal microbiota. Fecal samples were collected from healthy kidney donors (n=15), preemptive renal transplant recipients (n=4) and dialysis patients (n=31). Markers of inflammation (CRP and IL-6) and intestinal permeability (D-lactate) were measured in plasma.Results: Patients with ESRD did not have a significantly decreased amount F. prauznitzii, E. rectale and Roseburia spp. or the BCoAT gene. Neither was there a significant correlation with CRP, IL-6 or D-lactate. On the individual level, there were some patients with decreased BCoAT levels and increased levels of CRP, IL-6 and D-lactate.Conclusions: Patients with ESRD do not have a decreased amount of the most abundant butyrate-producing species nor a decreased butyrate-producing capacity.Keywords: renal failure, intestinal barrier function, butyrate, intestinal microbiota, inflammation renal failure intestinal barrier function butyrate intestinal microbiota inflammation Diseases of the genitourinary system. Urology Sinnige MJ verfasserin aut Hugenholtz F verfasserin aut Peters-Sengers H verfasserin aut Remmerswaal EBM verfasserin aut Geerlings SE verfasserin aut Bemelman FJ verfasserin aut In International Journal of Nephrology and Renovascular Disease Dove Medical Press, 2009 (2019), Seite 87-101 (DE-627)606031928 (DE-600)2508160-3 11787058 nnns year:2019 pages:87-101 https://doaj.org/article/cf2d53d55fee4d198916ddcd0a03fbda kostenfrei https://www.dovepress.com/butyrate-production-in-patients-with-end-stage-renal-disease-peer-reviewed-article-IJNRD kostenfrei https://doaj.org/toc/1178-7058 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 2019 87-101 |
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Butyrate production in patients with end-stage renal disease |
abstract |
Matty L Terpstra,1–3 Marjan J Sinnige,1,3 Floor Hugenholtz,4 Hessel Peters-Sengers,4 Ester BM Remmerswaal,1,3 Suzanne E Geerlings,2 Frederike J Bemelman11Department of Internal Medicine, Division of Nephrology, Renal Transplant Unit, Amsterdam UMC, University of Amsterdam, Amsterdam, Netherlands; 2Department of Internal Medicine, Division of Infectious Diseases, Amsterdam Infection & Immunity Institute (AI&II), Amsterdam UMC, University of Amsterdam, Amsterdam, The Netherlands; 3Department of Experimental Immunology, Amsterdam Infection & Immunity Institute (AI&II), Amsterdam UMC, University of Amsterdam, Amsterdam, The Netherlands; 4Center for Experimental and Molecular Medicine, Amsterdam UMC, University of Amsterdam, Amsterdam, NetherlandsBackground: Chronic kidney disease (CKD) is associated with a decreased intestinal barrier function, causing bacterial translocation over the intestinal wall and triggering a systemic inflammatory response. Butyrate, a short-chain fatty acid produced by certain bacterial strains, is considered instrumental to keep the intestinal barrier intact. There are indications that a decreased amount of these specific bacterial species is part of the cause of the decreased intestinal barrier function in CKD. The aim of this study is (i) to determine if Dutch patients with end-stage renal disease (ESRD) have a decreased amount of butyrate-producing species and butyrate-producing capacity and (ii) whether this correlates with systemic inflammation.Methods: We used qPCR to evaluate the most abundant butyrate-producing species F. prauznitzii, E. rectale and Roseburia spp. and the BCoAT gene, which reflects the butyrogenic capacity of the intestinal microbiota. Fecal samples were collected from healthy kidney donors (n=15), preemptive renal transplant recipients (n=4) and dialysis patients (n=31). Markers of inflammation (CRP and IL-6) and intestinal permeability (D-lactate) were measured in plasma.Results: Patients with ESRD did not have a significantly decreased amount F. prauznitzii, E. rectale and Roseburia spp. or the BCoAT gene. Neither was there a significant correlation with CRP, IL-6 or D-lactate. On the individual level, there were some patients with decreased BCoAT levels and increased levels of CRP, IL-6 and D-lactate.Conclusions: Patients with ESRD do not have a decreased amount of the most abundant butyrate-producing species nor a decreased butyrate-producing capacity.Keywords: renal failure, intestinal barrier function, butyrate, intestinal microbiota, inflammation |
abstractGer |
Matty L Terpstra,1–3 Marjan J Sinnige,1,3 Floor Hugenholtz,4 Hessel Peters-Sengers,4 Ester BM Remmerswaal,1,3 Suzanne E Geerlings,2 Frederike J Bemelman11Department of Internal Medicine, Division of Nephrology, Renal Transplant Unit, Amsterdam UMC, University of Amsterdam, Amsterdam, Netherlands; 2Department of Internal Medicine, Division of Infectious Diseases, Amsterdam Infection & Immunity Institute (AI&II), Amsterdam UMC, University of Amsterdam, Amsterdam, The Netherlands; 3Department of Experimental Immunology, Amsterdam Infection & Immunity Institute (AI&II), Amsterdam UMC, University of Amsterdam, Amsterdam, The Netherlands; 4Center for Experimental and Molecular Medicine, Amsterdam UMC, University of Amsterdam, Amsterdam, NetherlandsBackground: Chronic kidney disease (CKD) is associated with a decreased intestinal barrier function, causing bacterial translocation over the intestinal wall and triggering a systemic inflammatory response. Butyrate, a short-chain fatty acid produced by certain bacterial strains, is considered instrumental to keep the intestinal barrier intact. There are indications that a decreased amount of these specific bacterial species is part of the cause of the decreased intestinal barrier function in CKD. The aim of this study is (i) to determine if Dutch patients with end-stage renal disease (ESRD) have a decreased amount of butyrate-producing species and butyrate-producing capacity and (ii) whether this correlates with systemic inflammation.Methods: We used qPCR to evaluate the most abundant butyrate-producing species F. prauznitzii, E. rectale and Roseburia spp. and the BCoAT gene, which reflects the butyrogenic capacity of the intestinal microbiota. Fecal samples were collected from healthy kidney donors (n=15), preemptive renal transplant recipients (n=4) and dialysis patients (n=31). Markers of inflammation (CRP and IL-6) and intestinal permeability (D-lactate) were measured in plasma.Results: Patients with ESRD did not have a significantly decreased amount F. prauznitzii, E. rectale and Roseburia spp. or the BCoAT gene. Neither was there a significant correlation with CRP, IL-6 or D-lactate. On the individual level, there were some patients with decreased BCoAT levels and increased levels of CRP, IL-6 and D-lactate.Conclusions: Patients with ESRD do not have a decreased amount of the most abundant butyrate-producing species nor a decreased butyrate-producing capacity.Keywords: renal failure, intestinal barrier function, butyrate, intestinal microbiota, inflammation |
abstract_unstemmed |
Matty L Terpstra,1–3 Marjan J Sinnige,1,3 Floor Hugenholtz,4 Hessel Peters-Sengers,4 Ester BM Remmerswaal,1,3 Suzanne E Geerlings,2 Frederike J Bemelman11Department of Internal Medicine, Division of Nephrology, Renal Transplant Unit, Amsterdam UMC, University of Amsterdam, Amsterdam, Netherlands; 2Department of Internal Medicine, Division of Infectious Diseases, Amsterdam Infection & Immunity Institute (AI&II), Amsterdam UMC, University of Amsterdam, Amsterdam, The Netherlands; 3Department of Experimental Immunology, Amsterdam Infection & Immunity Institute (AI&II), Amsterdam UMC, University of Amsterdam, Amsterdam, The Netherlands; 4Center for Experimental and Molecular Medicine, Amsterdam UMC, University of Amsterdam, Amsterdam, NetherlandsBackground: Chronic kidney disease (CKD) is associated with a decreased intestinal barrier function, causing bacterial translocation over the intestinal wall and triggering a systemic inflammatory response. Butyrate, a short-chain fatty acid produced by certain bacterial strains, is considered instrumental to keep the intestinal barrier intact. There are indications that a decreased amount of these specific bacterial species is part of the cause of the decreased intestinal barrier function in CKD. The aim of this study is (i) to determine if Dutch patients with end-stage renal disease (ESRD) have a decreased amount of butyrate-producing species and butyrate-producing capacity and (ii) whether this correlates with systemic inflammation.Methods: We used qPCR to evaluate the most abundant butyrate-producing species F. prauznitzii, E. rectale and Roseburia spp. and the BCoAT gene, which reflects the butyrogenic capacity of the intestinal microbiota. Fecal samples were collected from healthy kidney donors (n=15), preemptive renal transplant recipients (n=4) and dialysis patients (n=31). Markers of inflammation (CRP and IL-6) and intestinal permeability (D-lactate) were measured in plasma.Results: Patients with ESRD did not have a significantly decreased amount F. prauznitzii, E. rectale and Roseburia spp. or the BCoAT gene. Neither was there a significant correlation with CRP, IL-6 or D-lactate. On the individual level, there were some patients with decreased BCoAT levels and increased levels of CRP, IL-6 and D-lactate.Conclusions: Patients with ESRD do not have a decreased amount of the most abundant butyrate-producing species nor a decreased butyrate-producing capacity.Keywords: renal failure, intestinal barrier function, butyrate, intestinal microbiota, inflammation |
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title_short |
Butyrate production in patients with end-stage renal disease |
url |
https://doaj.org/article/cf2d53d55fee4d198916ddcd0a03fbda https://www.dovepress.com/butyrate-production-in-patients-with-end-stage-renal-disease-peer-reviewed-article-IJNRD https://doaj.org/toc/1178-7058 |
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